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For: Lippai D, Bala S, Catalano D, Kodys K, Szabo G. Micro-RNA-155 deficiency prevents alcohol-induced serum endotoxin increase and small bowel inflammation in mice. Alcohol Clin Exp Res 2015;38:2217-24. [PMID: 25156614 DOI: 10.1111/acer.12483] [Citation(s) in RCA: 82] [Impact Index Per Article: 8.2] [Reference Citation Analysis] [What about the content of this article? (0)] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 08/23/2013] [Accepted: 04/29/2014] [Indexed: 02/07/2023]

For:	Lippai D, Bala S, Catalano D, Kodys K, Szabo G. Micro-RNA-155 deficiency prevents alcohol-induced serum endotoxin increase and small bowel inflammation in mice. Alcohol Clin Exp Res 2015;38:2217-24. [PMID: 25156614 DOI: 10.1111/acer.12483] [Citation(s) in RCA: 82] [Impact Index Per Article: 8.2] [Reference Citation Analysis] [What about the content of this article? (0)] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 08/23/2013] [Accepted: 04/29/2014] [Indexed: 02/07/2023]

Number

Cited by Other Article(s)

Chen L, Tang J, Xia Y, Wang J, Xia LN. Mechanistic study of the effect of a high-salt diet on the intestinal barrier. Sci Rep 2025;15:3826. [PMID: 39885261 PMCID: PMC11782509 DOI: 10.1038/s41598-025-88291-y] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Grants] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 07/01/2024] [Accepted: 01/28/2025] [Indexed: 02/01/2025] Open

Calvez V, Puca P, Di Vincenzo F, Del Gaudio A, Bartocci B, Murgiano M, Iaccarino J, Parand E, Napolitano D, Pugliese D, Gasbarrini A, Scaldaferri F. Novel Insights into the Pathogenesis of Inflammatory Bowel Diseases. Biomedicines 2025;13:305. [PMID: 40002718 PMCID: PMC11853239 DOI: 10.3390/biomedicines13020305] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 12/07/2024] [Revised: 01/17/2025] [Accepted: 01/21/2025] [Indexed: 02/27/2025] Open

Affiliation(s)

Valentin Calvez IBD Unit, UOC CEMAD Medicina Interna e Gastroenterologia, Centro Malattie dell’Apparato Digerente, Dipartimento di Scienze Mediche e Chirurgiche Addominali ed Endocrino Metaboliche, Fondazione Policlinico Universitario Agostino Gemelli IRCCS, 00168 Rome, Italy; (V.C.); (P.P.); (D.N.); (D.P.) Dipartimento di Medicina e Chirurgia Traslazionale, Università Cattolica del Sacro Cuore, 00168 Rome, Italy; (F.D.V.); (A.D.G.); (B.B.); (M.M.); (J.I.); (E.P.); (A.G.)
Pierluigi Puca IBD Unit, UOC CEMAD Medicina Interna e Gastroenterologia, Centro Malattie dell’Apparato Digerente, Dipartimento di Scienze Mediche e Chirurgiche Addominali ed Endocrino Metaboliche, Fondazione Policlinico Universitario Agostino Gemelli IRCCS, 00168 Rome, Italy; (V.C.); (P.P.); (D.N.); (D.P.) Dipartimento di Medicina e Chirurgia Traslazionale, Università Cattolica del Sacro Cuore, 00168 Rome, Italy; (F.D.V.); (A.D.G.); (B.B.); (M.M.); (J.I.); (E.P.); (A.G.)
Federica Di Vincenzo Dipartimento di Medicina e Chirurgia Traslazionale, Università Cattolica del Sacro Cuore, 00168 Rome, Italy; (F.D.V.); (A.D.G.); (B.B.); (M.M.); (J.I.); (E.P.); (A.G.)
Angelo Del Gaudio Dipartimento di Medicina e Chirurgia Traslazionale, Università Cattolica del Sacro Cuore, 00168 Rome, Italy; (F.D.V.); (A.D.G.); (B.B.); (M.M.); (J.I.); (E.P.); (A.G.)
Bianca Bartocci Dipartimento di Medicina e Chirurgia Traslazionale, Università Cattolica del Sacro Cuore, 00168 Rome, Italy; (F.D.V.); (A.D.G.); (B.B.); (M.M.); (J.I.); (E.P.); (A.G.)
Marco Murgiano Dipartimento di Medicina e Chirurgia Traslazionale, Università Cattolica del Sacro Cuore, 00168 Rome, Italy; (F.D.V.); (A.D.G.); (B.B.); (M.M.); (J.I.); (E.P.); (A.G.)
Jacopo Iaccarino Dipartimento di Medicina e Chirurgia Traslazionale, Università Cattolica del Sacro Cuore, 00168 Rome, Italy; (F.D.V.); (A.D.G.); (B.B.); (M.M.); (J.I.); (E.P.); (A.G.)
Erfan Parand Dipartimento di Medicina e Chirurgia Traslazionale, Università Cattolica del Sacro Cuore, 00168 Rome, Italy; (F.D.V.); (A.D.G.); (B.B.); (M.M.); (J.I.); (E.P.); (A.G.)
Daniele Napolitano IBD Unit, UOC CEMAD Medicina Interna e Gastroenterologia, Centro Malattie dell’Apparato Digerente, Dipartimento di Scienze Mediche e Chirurgiche Addominali ed Endocrino Metaboliche, Fondazione Policlinico Universitario Agostino Gemelli IRCCS, 00168 Rome, Italy; (V.C.); (P.P.); (D.N.); (D.P.)
Daniela Pugliese IBD Unit, UOC CEMAD Medicina Interna e Gastroenterologia, Centro Malattie dell’Apparato Digerente, Dipartimento di Scienze Mediche e Chirurgiche Addominali ed Endocrino Metaboliche, Fondazione Policlinico Universitario Agostino Gemelli IRCCS, 00168 Rome, Italy; (V.C.); (P.P.); (D.N.); (D.P.) Dipartimento di Medicina e Chirurgia Traslazionale, Università Cattolica del Sacro Cuore, 00168 Rome, Italy; (F.D.V.); (A.D.G.); (B.B.); (M.M.); (J.I.); (E.P.); (A.G.)
Antonio Gasbarrini Dipartimento di Medicina e Chirurgia Traslazionale, Università Cattolica del Sacro Cuore, 00168 Rome, Italy; (F.D.V.); (A.D.G.); (B.B.); (M.M.); (J.I.); (E.P.); (A.G.)
Franco Scaldaferri IBD Unit, UOC CEMAD Medicina Interna e Gastroenterologia, Centro Malattie dell’Apparato Digerente, Dipartimento di Scienze Mediche e Chirurgiche Addominali ed Endocrino Metaboliche, Fondazione Policlinico Universitario Agostino Gemelli IRCCS, 00168 Rome, Italy; (V.C.); (P.P.); (D.N.); (D.P.) Dipartimento di Medicina e Chirurgia Traslazionale, Università Cattolica del Sacro Cuore, 00168 Rome, Italy; (F.D.V.); (A.D.G.); (B.B.); (M.M.); (J.I.); (E.P.); (A.G.)

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Termite F, Archilei S, D’Ambrosio F, Petrucci L, Viceconti N, Iaccarino R, Liguori A, Gasbarrini A, Miele L. Gut Microbiota at the Crossroad of Hepatic Oxidative Stress and MASLD. Antioxidants (Basel) 2025;14:56. [PMID: 39857390 PMCID: PMC11759774 DOI: 10.3390/antiox14010056] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 12/13/2024] [Revised: 12/30/2024] [Accepted: 01/02/2025] [Indexed: 01/27/2025] Open

Su J, Dai Y, Wu X, Zhou X, Fang X, Ge X, Zhao L. Maslinic acid alleviates alcoholic liver injury in mice and regulates intestinal microbiota via the gut-liver axis. JOURNAL OF THE SCIENCE OF FOOD AND AGRICULTURE 2024;104:7928-7938. [PMID: 38837352 DOI: 10.1002/jsfa.13624] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Subscribe] [Scholar Register] [Received: 12/05/2023] [Revised: 04/01/2024] [Accepted: 05/20/2024] [Indexed: 06/07/2024]

Zhang M, Wang Y, Gan Y. The potential role of Akkermansia muciniphila in liver health. Future Microbiol 2024;19:1081-1096. [PMID: 39109507 PMCID: PMC11323942 DOI: 10.2217/fmb-2023-0220] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Grants] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 08/15/2024] Open

Turner BRH, Jenkinson PI, Huttman M, Mullish BH. Inflammation, oxidative stress and gut microbiome perturbation: A narrative review of mechanisms and treatment of the alcohol hangover. ALCOHOL, CLINICAL & EXPERIMENTAL RESEARCH 2024;48:1451-1465. [PMID: 38965644 DOI: 10.1111/acer.15396] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Subscribe] [Scholar Register] [Received: 04/11/2024] [Revised: 05/17/2024] [Accepted: 06/03/2024] [Indexed: 07/06/2024]

Abstract

Alcohol is the most widely abused substance in the world, the leading source of mortality in 15-49-year-olds, and a major risk factor for heart disease, liver disease, diabetes, and cancer. Despite this, alcohol is regularly misused in wider society. Consumers of excess alcohol often note a constellation of negative symptoms, known as the alcohol hangover. However, the alcohol hangover is not considered to have long-term clinical significance by clinicians or consumers. We undertook a critical review of the literature to demonstrate the pathophysiological mechanisms of the alcohol hangover. Hereafter, the alcohol hangover is re-defined as a manifestation of sickness behavior secondary to alcohol-induced inflammation, using the Bradford-Hill criteria to demonstrate causation above correlation. Alcohol causes inflammation through oxidative stress and endotoxemia. Alcohol metabolism is oxidative and increased intake causes relative tissue hypoxia and increased free radical generation. Tissue damage ensues through lipid peroxidation and the formation of DNA/protein adducts. Byproducts of alcohol metabolism such as acetaldehyde and congeners, sleep deprivation, and the activation of nonspecific inducible CYP2E1 in alcohol-exposed tissues exacerbate free radical generation. Tissue damage and cell death lead to inflammation, but in the intestine loss of epithelial cells leads to intestinal permeability, allowing the translocation of pathogenic bacteria to the systemic circulation (endotoxemia). This leads to a well-characterized cascade of systemic inflammation, additionally activating toll-like receptor 4 to induce sickness behavior. Considering the evidence, it is suggested that hangover frequency and severity may be predictors of the development of later alcohol-related diseases, meriting formal confirmation in prospective studies. In light of the mechanisms of alcohol-mediated inflammation, research into gut permeability and the gut microbiome may be an exciting future therapeutic avenue to prevent alcohol hangover and other alcohol-related diseases.

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Du M, Liu Y, Cao J, Li X, Wang N, He Q, Zhang L, Zhao B, Dugarjaviin M. Food from Equids-Commercial Fermented Mare's Milk (Koumiss) Products: Protective Effects against Alcohol Intoxication. Foods 2024;13:2344. [PMID: 39123538 PMCID: PMC11312395 DOI: 10.3390/foods13152344] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [Grants] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 06/29/2024] [Revised: 07/19/2024] [Accepted: 07/22/2024] [Indexed: 08/12/2024] Open

Affiliation(s)

Ming Du Key Laboratory of Equus Germplasm Innovation, Ministry of Agriculture and Rural Affairs, Hohhot 010018, China; (M.D.); (Y.L.); (J.C.); (X.L.); (N.W.); (Q.H.); (L.Z.); (B.Z.) Inner Mongolia Key Laboratory of Equine Science Research and Technology Innovation, Inner Mongolia Agricultural University, Hohhot 010018, China Equus Research Center, Inner Mongolia Agricultural University, Hohhot 010018, China
Yuanyi Liu Key Laboratory of Equus Germplasm Innovation, Ministry of Agriculture and Rural Affairs, Hohhot 010018, China; (M.D.); (Y.L.); (J.C.); (X.L.); (N.W.); (Q.H.); (L.Z.); (B.Z.) Inner Mongolia Key Laboratory of Equine Science Research and Technology Innovation, Inner Mongolia Agricultural University, Hohhot 010018, China Equus Research Center, Inner Mongolia Agricultural University, Hohhot 010018, China
Jialong Cao Key Laboratory of Equus Germplasm Innovation, Ministry of Agriculture and Rural Affairs, Hohhot 010018, China; (M.D.); (Y.L.); (J.C.); (X.L.); (N.W.); (Q.H.); (L.Z.); (B.Z.) Inner Mongolia Key Laboratory of Equine Science Research and Technology Innovation, Inner Mongolia Agricultural University, Hohhot 010018, China Equus Research Center, Inner Mongolia Agricultural University, Hohhot 010018, China
Xinyu Li Key Laboratory of Equus Germplasm Innovation, Ministry of Agriculture and Rural Affairs, Hohhot 010018, China; (M.D.); (Y.L.); (J.C.); (X.L.); (N.W.); (Q.H.); (L.Z.); (B.Z.) Inner Mongolia Key Laboratory of Equine Science Research and Technology Innovation, Inner Mongolia Agricultural University, Hohhot 010018, China Equus Research Center, Inner Mongolia Agricultural University, Hohhot 010018, China
Na Wang Key Laboratory of Equus Germplasm Innovation, Ministry of Agriculture and Rural Affairs, Hohhot 010018, China; (M.D.); (Y.L.); (J.C.); (X.L.); (N.W.); (Q.H.); (L.Z.); (B.Z.) Inner Mongolia Key Laboratory of Equine Science Research and Technology Innovation, Inner Mongolia Agricultural University, Hohhot 010018, China Equus Research Center, Inner Mongolia Agricultural University, Hohhot 010018, China
Qianqian He Key Laboratory of Equus Germplasm Innovation, Ministry of Agriculture and Rural Affairs, Hohhot 010018, China; (M.D.); (Y.L.); (J.C.); (X.L.); (N.W.); (Q.H.); (L.Z.); (B.Z.) Inner Mongolia Key Laboratory of Equine Science Research and Technology Innovation, Inner Mongolia Agricultural University, Hohhot 010018, China Equus Research Center, Inner Mongolia Agricultural University, Hohhot 010018, China
Lei Zhang Key Laboratory of Equus Germplasm Innovation, Ministry of Agriculture and Rural Affairs, Hohhot 010018, China; (M.D.); (Y.L.); (J.C.); (X.L.); (N.W.); (Q.H.); (L.Z.); (B.Z.) Inner Mongolia Key Laboratory of Equine Science Research and Technology Innovation, Inner Mongolia Agricultural University, Hohhot 010018, China Equus Research Center, Inner Mongolia Agricultural University, Hohhot 010018, China
Bilig Zhao Key Laboratory of Equus Germplasm Innovation, Ministry of Agriculture and Rural Affairs, Hohhot 010018, China; (M.D.); (Y.L.); (J.C.); (X.L.); (N.W.); (Q.H.); (L.Z.); (B.Z.) Inner Mongolia Key Laboratory of Equine Science Research and Technology Innovation, Inner Mongolia Agricultural University, Hohhot 010018, China Equus Research Center, Inner Mongolia Agricultural University, Hohhot 010018, China
Manglai Dugarjaviin Key Laboratory of Equus Germplasm Innovation, Ministry of Agriculture and Rural Affairs, Hohhot 010018, China; (M.D.); (Y.L.); (J.C.); (X.L.); (N.W.); (Q.H.); (L.Z.); (B.Z.) Inner Mongolia Key Laboratory of Equine Science Research and Technology Innovation, Inner Mongolia Agricultural University, Hohhot 010018, China Equus Research Center, Inner Mongolia Agricultural University, Hohhot 010018, China

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Bai Y, Liu F, Zheng L, Wan Y, Fan J, Deng J, Li Q, Xie Y, Guo P. "Yajieshaba" prevents acute alcoholic liver injury and repairs the intestinal mucosal barrier. JOURNAL OF ETHNOPHARMACOLOGY 2024;318:116921. [PMID: 37490990 DOI: 10.1016/j.jep.2023.116921] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Subscribe] [Scholar Register] [Received: 03/31/2023] [Revised: 05/12/2023] [Accepted: 07/13/2023] [Indexed: 07/27/2023]

Abstract

ETHNOPHARMACOLOGICAL RELEVANCE

An essential factor related to the acute alcoholic liver injury is damage to the intestinal mucosal barrier. Yajieshaba (YJSB) is a commonly used formulation of Dai people in China and protects the liver.

AIM OF THE STUDY

This study investigated whether YJSB can prevent acute alcoholic liver injury by regulating the intestinal mucosal barrier.

MATERIALS AND METHODS

The mice received 0.39 g/kg, 1.17 g/kg, and 3.51 g/kg dose YJSB for 7 days, a mouse model of acute alcoholic liver injury was established by a single instillation of 56% alcohol. Plasma biochemical markers were analyzed, liver injury was identified by histopathology, lipopolysaccharide (LPS), nuclear factor-k-gene binding (NF-κB), hepatic inflammatory factors, oxidative stress factors and reactive oxygen species (ROS) content was analyzed. The morphological changes of intestinal histology were observed by H&E staining, and the ultrastructure of ileal cells was observed by transmission electron microscopy. Immunofluorescence and Western blot was used to determine the expression levels of transporters and enzymes involved in Claudin 1, Occludin and zona occludens 1 (ZO-1) homeostasis in the liver and intestine.

RESULTS

The findings showed that YJSB reduced the levels of aspartate aminotr ansferase (AST), alanine aminotransferase (ALT) and total bile acid (TBA), both of which are indicators of liver function and had a protective effect against liver injury. In the liver homogenate, YJSB reduced the level of LPS, NF-κB, tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β) and interleukin-6 (IL-6), decreased the level of superoxide dismutase (SOD), malondialdehyde (MDA), glutathione peroxidase (GSH-PX) and catalase (CAT) and ROS. The results of hematoxylin and eosin (H&E) staining and transmission electron microscopy analysis revealed that YJSB reduced the degree of damage to intestinal tissue and intracellular organelles, implying that YJSB can reduce the "attack factor" that causes intestinal barrier damage, increase the "defense factor" that protects the intestinal barrier. The results of immunohistochemistry and Western blotting analysis showed that YJSB could increase the expression of claudin 1, occludin, and ZO-1 proteins, suggesting that the mechanism of action of YJSB against acute alcohol liver injury involves the upregulation of the expression of the intestinal barrier-related proteins and the repair of the damaged intestinal barrier.

CONCLUSIONS

YJSB can block LPS, oxidative stress factors, and other harmful substances in the blood and protect the liver resisting acute alcoholic liver injury.

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Yang K, Song M. New Insights into the Pathogenesis of Metabolic-Associated Fatty Liver Disease (MAFLD): Gut-Liver-Heart Crosstalk. Nutrients 2023;15:3970. [PMID: 37764755 PMCID: PMC10534946 DOI: 10.3390/nu15183970] [Citation(s) in RCA: 20] [Impact Index Per Article: 10.0] [Reference Citation Analysis] [Abstract] [Key Words] [Grants] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 08/21/2023] [Revised: 09/11/2023] [Accepted: 09/13/2023] [Indexed: 09/29/2023] Open

Zhang D, Liu Z, Bai F. Roles of Gut Microbiota in Alcoholic Liver Disease. Int J Gen Med 2023;16:3735-3746. [PMID: 37641627 PMCID: PMC10460590 DOI: 10.2147/ijgm.s420195] [Citation(s) in RCA: 13] [Impact Index Per Article: 6.5] [Reference Citation Analysis] [Abstract] [Key Words] [Grants] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 05/06/2023] [Accepted: 08/10/2023] [Indexed: 08/31/2023] Open

Odriozola A, Santos-Laso A, Del Barrio M, Cabezas J, Iruzubieta P, Arias-Loste MT, Rivas C, Duque JCR, Antón Á, Fábrega E, Crespo J. Fatty Liver Disease, Metabolism and Alcohol Interplay: A Comprehensive Review. Int J Mol Sci 2023;24:ijms24097791. [PMID: 37175497 PMCID: PMC10178387 DOI: 10.3390/ijms24097791] [Citation(s) in RCA: 5] [Impact Index Per Article: 2.5] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 02/21/2023] [Revised: 04/05/2023] [Accepted: 04/07/2023] [Indexed: 05/15/2023] Open

Affiliation(s)

Aitor Odriozola Gastroenterology and Hepatology Department, Clinical and Translational Research in Digestive Diseases, Valdecilla Research Institute (IDIVAL), Marqués de Valdecilla Universitary Hospital, Av. Valdecilla 25, 39008 Santander, Cantabria, Spain
Alvaro Santos-Laso Gastroenterology and Hepatology Department, Clinical and Translational Research in Digestive Diseases, Valdecilla Research Institute (IDIVAL), Marqués de Valdecilla Universitary Hospital, Av. Valdecilla 25, 39008 Santander, Cantabria, Spain
María Del Barrio Gastroenterology and Hepatology Department, Clinical and Translational Research in Digestive Diseases, Valdecilla Research Institute (IDIVAL), Marqués de Valdecilla Universitary Hospital, Av. Valdecilla 25, 39008 Santander, Cantabria, Spain
Joaquín Cabezas Gastroenterology and Hepatology Department, Clinical and Translational Research in Digestive Diseases, Valdecilla Research Institute (IDIVAL), Marqués de Valdecilla Universitary Hospital, Av. Valdecilla 25, 39008 Santander, Cantabria, Spain
Paula Iruzubieta Gastroenterology and Hepatology Department, Clinical and Translational Research in Digestive Diseases, Valdecilla Research Institute (IDIVAL), Marqués de Valdecilla Universitary Hospital, Av. Valdecilla 25, 39008 Santander, Cantabria, Spain
María Teresa Arias-Loste Gastroenterology and Hepatology Department, Clinical and Translational Research in Digestive Diseases, Valdecilla Research Institute (IDIVAL), Marqués de Valdecilla Universitary Hospital, Av. Valdecilla 25, 39008 Santander, Cantabria, Spain
Coral Rivas Gastroenterology and Hepatology Department, Clinical and Translational Research in Digestive Diseases, Valdecilla Research Institute (IDIVAL), Marqués de Valdecilla Universitary Hospital, Av. Valdecilla 25, 39008 Santander, Cantabria, Spain
Juan Carlos Rodríguez Duque Gastroenterology and Hepatology Department, Clinical and Translational Research in Digestive Diseases, Valdecilla Research Institute (IDIVAL), Marqués de Valdecilla Universitary Hospital, Av. Valdecilla 25, 39008 Santander, Cantabria, Spain
Ángela Antón Gastroenterology and Hepatology Department, Clinical and Translational Research in Digestive Diseases, Valdecilla Research Institute (IDIVAL), Marqués de Valdecilla Universitary Hospital, Av. Valdecilla 25, 39008 Santander, Cantabria, Spain
Emilio Fábrega Gastroenterology and Hepatology Department, Clinical and Translational Research in Digestive Diseases, Valdecilla Research Institute (IDIVAL), Marqués de Valdecilla Universitary Hospital, Av. Valdecilla 25, 39008 Santander, Cantabria, Spain
Javier Crespo Gastroenterology and Hepatology Department, Clinical and Translational Research in Digestive Diseases, Valdecilla Research Institute (IDIVAL), Marqués de Valdecilla Universitary Hospital, Av. Valdecilla 25, 39008 Santander, Cantabria, Spain

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Liu X, Yu S, Zhang Y, Zhang W, Zhong H, Lu X, Guan R. A review on the protective effect of active components in Antrodia camphorata against alcoholic liver injury. JOURNAL OF ETHNOPHARMACOLOGY 2023;300:115740. [PMID: 36162549 DOI: 10.1016/j.jep.2022.115740] [Citation(s) in RCA: 2] [Impact Index Per Article: 1.0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Subscribe] [Scholar Register] [Received: 06/29/2022] [Revised: 09/02/2022] [Accepted: 09/15/2022] [Indexed: 06/16/2023]

Abstract

ETHNOPHARMACOLOGICAL RELEVANCE

Antrodia camphorata is a genus of wood-rot basidiomycete in the family Fomitopsidaceae. It is a valuable medicinal fungus in China that contains more than 78 kinds of active compounds. A. camphorata has good protection effects on the liver, especially on alcoholic liver injury (ALI).

AIM

This paper summarizes the complex occurrence and development of alcoholic liver disease (ALD). In addition, the effect of ALD on the intestine through the gut-liver axis is summarized. The protective mechanism of A. camphorata on ALI is reviewed to reveal its therapeutic potential, offering insights into future research.

MATERIALS AND METHODS

A comprehensive search in the literature was obtained from books and online databases such as Web of Science, Google Scholar, PubMed, Scopus, Science direct, ACS Publications and Baidu Scholar.

RESULTS

The pathogenesis of ALD mainly includes oxidative stress injury, intestinal microflora imbalance, inflammatory mediator injury and nutritional imbalance. A. camphorata contains rich active components (e.g. polysaccharides, triterpenoids, maleic and succinic acid derivatives, amino acids, superoxide dismutase, vitamins, lignin and sterols). These components have good antioxidant, anti-inflammatory and intestinal protection activities. Therefore, A. camphorata has a wide application in the prevention and treatment of ALI.

CONCLUSIONS

ALD develops from a mild disease to alcoholic hepatitis and cirrhosis, which is the main reason of global morbidity and mortality. At present, there is no effective drug for the treatment of ALD. A. camphorata, as a valuable medicinal fungus unique to Taiwan, has a great protective effect on the liver. It is expected to be an effective drug for ALI treatment. Although many studies have performed the protective effects of A. camphorata on ALI, its regulatory effects on the gut-liver axis of ALD patients need to be further explored.

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Chen G, Shi F, Yin W, Guo Y, Liu A, Shuai J, Sun J. Gut microbiota dysbiosis: The potential mechanisms by which alcohol disrupts gut and brain functions. Front Microbiol 2022;13:916765. [PMID: 35966709 PMCID: PMC9372561 DOI: 10.3389/fmicb.2022.916765] [Citation(s) in RCA: 4] [Impact Index Per Article: 1.3] [Reference Citation Analysis] [Abstract] [Grants] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 04/11/2022] [Accepted: 06/29/2022] [Indexed: 11/24/2022] Open

Vieujean S, Caron B, Haghnejad V, Jouzeau JY, Netter P, Heba AC, Ndiaye NC, Moulin D, Barreto G, Danese S, Peyrin-Biroulet L. Impact of the Exposome on the Epigenome in Inflammatory Bowel Disease Patients and Animal Models. Int J Mol Sci 2022;23:7611. [PMID: 35886959 PMCID: PMC9321337 DOI: 10.3390/ijms23147611] [Citation(s) in RCA: 15] [Impact Index Per Article: 5.0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Grants] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 05/31/2022] [Revised: 07/05/2022] [Accepted: 07/06/2022] [Indexed: 02/07/2023] Open

Abstract

Inflammatory bowel diseases (IBD) are chronic inflammatory disorders of the gastrointestinal tract that encompass two main phenotypes, namely Crohn's disease and ulcerative colitis. These conditions occur in genetically predisposed individuals in response to environmental factors. Epigenetics, acting by DNA methylation, post-translational histones modifications or by non-coding RNAs, could explain how the exposome (or all environmental influences over the life course, from conception to death) could influence the gene expression to contribute to intestinal inflammation. We performed a scoping search using Medline to identify all the elements of the exposome that may play a role in intestinal inflammation through epigenetic modifications, as well as the underlying mechanisms. The environmental factors epigenetically influencing the occurrence of intestinal inflammation are the maternal lifestyle (mainly diet, the occurrence of infection during pregnancy and smoking); breastfeeding; microbiota; diet (including a low-fiber diet, high-fat diet and deficiency in micronutrients); smoking habits, vitamin D and drugs (e.g., IBD treatments, antibiotics and probiotics). Influenced by both microbiota and diet, short-chain fatty acids are gut microbiota-derived metabolites resulting from the anaerobic fermentation of non-digestible dietary fibers, playing an epigenetically mediated role in the integrity of the epithelial barrier and in the defense against invading microorganisms. Although the impact of some environmental factors has been identified, the exposome-induced epimutations in IBD remain a largely underexplored field. How these environmental exposures induce epigenetic modifications (in terms of duration, frequency and the timing at which they occur) and how other environmental factors associated with IBD modulate epigenetics deserve to be further investigated.

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Affiliation(s)

Sophie Vieujean Hepato-Gastroenterology and Digestive Oncology, University Hospital CHU of Liège, 4000 Liege, Belgium;
Bénédicte Caron Department of Gastroenterology NGERE (INSERM U1256), Nancy University Hospital, University of Lorraine, Vandœuvre-lès-Nancy, F-54052 Nancy, France; (B.C.); (V.H.)
Vincent Haghnejad Department of Gastroenterology NGERE (INSERM U1256), Nancy University Hospital, University of Lorraine, Vandœuvre-lès-Nancy, F-54052 Nancy, France; (B.C.); (V.H.)
Jean-Yves Jouzeau CNRS (French National Centre for Scientific Research), Laboratoire IMoPA, Université de Lorraine, UMR 7365, F-54000 Nancy, France; (J.-Y.J.); (P.N.); (D.M.); (G.B.)
Patrick Netter CNRS (French National Centre for Scientific Research), Laboratoire IMoPA, Université de Lorraine, UMR 7365, F-54000 Nancy, France; (J.-Y.J.); (P.N.); (D.M.); (G.B.)
Anne-Charlotte Heba NGERE (Nutrition-Genetics and Exposure to Environmental Risks), National Institute of Health and Medical Research, University of Lorraine, F-54000 Nancy, France; (A.-C.H.); (N.C.N.)
Ndeye Coumba Ndiaye NGERE (Nutrition-Genetics and Exposure to Environmental Risks), National Institute of Health and Medical Research, University of Lorraine, F-54000 Nancy, France; (A.-C.H.); (N.C.N.)
David Moulin CNRS (French National Centre for Scientific Research), Laboratoire IMoPA, Université de Lorraine, UMR 7365, F-54000 Nancy, France; (J.-Y.J.); (P.N.); (D.M.); (G.B.)
Guillermo Barreto CNRS (French National Centre for Scientific Research), Laboratoire IMoPA, Université de Lorraine, UMR 7365, F-54000 Nancy, France; (J.-Y.J.); (P.N.); (D.M.); (G.B.) Lung Cancer Epigenetics, Max-Planck-Institute for Heart and Lung Research, 61231 Bad Nauheim, Germany International Laboratory EPIGEN, Consejo de Ciencia y Tecnología del Estado de Puebla (CONCYTEP), Universidad de la Salud del Estado de Puebla, Puebla 72000, Mexico
Silvio Danese Gastroenterology and Endoscopy, IRCCS Ospedale San Raffaele and University Vita-Salute San Raffaele, 20132 Milan, Italy;
Laurent Peyrin-Biroulet Department of Gastroenterology NGERE (INSERM U1256), Nancy University Hospital, University of Lorraine, Vandœuvre-lès-Nancy, F-54052 Nancy, France; (B.C.); (V.H.)

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Wang C, Li S, Liu Q, Qian Q, Fu A, Chen L, Zhang L, Suzaki T, Yu Z, Dou X. Ectopic accumulation of ceramide in cardiomyocytes modulates alcoholic cardiomyopathy via the TLR4-dependent pathway. Alcohol Clin Exp Res 2022;46:1011-1022. [PMID: 35373347 DOI: 10.1111/acer.14822] [Citation(s) in RCA: 1] [Impact Index Per Article: 0.3] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 12/17/2021] [Revised: 03/23/2022] [Accepted: 03/25/2022] [Indexed: 12/26/2022]

Abstract

BACKGROUND AND AIMS

Excessive alcohol consumption predisposes drinkers to develop alcoholic cardiomyopathy. Although cardiomyocyte loss is the hallmark of cardiomyopathy, the underlying mechanism remains elusive. This study examined the potential mechanism of alcohol-induced cardiomyocyte death in a mouse model of alcoholic cardiomyopathy.

METHODS

We established the alcoholic cardiomyopathy mouse model using C57BL/6J mice and confirmed it via echocardiography and histological examination. The cardiac ceramide content and profile were analyzed with a triple-quadrupole mass spectrometer. The molecular mechanism underlying the accumulation of ceramide due to chronic alcohol consumption and ceramide-induced cardiomyocyte death were investigated by in vivo and in vitro models. Finally, we established a TLR4 mutation model to explore the function of TLR4 in CH3/HeJ mice.

RESULTS

Cardiac lipotoxicity that followed alcohol exposure resulted mainly in C16:0-, C18:0-, and C24:1-ceramide aggregation. Genes encoding the sphingosine hydrolysis enzymes (SMPD1 and SMPD2) rather than de novo synthetic biomarkers were markedly upregulated. Exogenous ceramide mimics (C6-ceramide) werenderlying the accumulation of ceramide observed to cause H9C2 cardiomyocyte-like cell death, which was consistent with results under palmate acid (PA) treatment. As a ceramide precursor, PA induces intracellular ceramide generation through TLR4 signaling, which can be abolished by an inhibitor of ceramide synthesis. Furthermore, mechanistic investigations demonstrated that pharmacological or genetic inhibition of TLR4 attenuated PA-induced cell death and corresponding ceramide production. Moreover, global mutation of TLR4 in CH3/HeJ mice significantly reduced the accumulation of C24:0, C24:1, OH_C24:1, and total ceramide following alcohol challenge.

CONCLUSIONS

Our findings demonstrate that ceramide accumulation plays a crucial role in alcoholic cardiomyopathy, effects that are partially mediated through the TLR4-dependent pathway.

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Xu Q, Zhang R, Mu Y, Song Y, Hao N, Wei Y, Wang Q, Mackay CR. Propionate Ameliorates Alcohol-Induced Liver Injury in Mice via the Gut-Liver Axis: Focus on the Improvement of Intestinal Permeability. JOURNAL OF AGRICULTURAL AND FOOD CHEMISTRY 2022;70:6084-6096. [PMID: 35549256 DOI: 10.1021/acs.jafc.2c00633] [Citation(s) in RCA: 28] [Impact Index Per Article: 9.3] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Subscribe] [Scholar Register] [Indexed: 06/15/2023]

Tian Y, Wang TS, Bu H, Shao G, Zhang W, Zhang L. Role of Exosomal miR-223 in Chronic Skeletal Muscle Inflammation. Orthop Surg 2022;14:644-651. [PMID: 35293669 PMCID: PMC9002075 DOI: 10.1111/os.13232] [Citation(s) in RCA: 1] [Impact Index Per Article: 0.3] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 05/16/2021] [Revised: 12/30/2021] [Accepted: 01/19/2022] [Indexed: 12/14/2022] Open

Habash NW, Sehrawat TS, Shah VH, Cao S. Epigenetics of alcohol-related liver diseases. JHEP REPORTS : INNOVATION IN HEPATOLOGY 2022;4:100466. [PMID: 35462859 PMCID: PMC9018389 DOI: 10.1016/j.jhepr.2022.100466] [Citation(s) in RCA: 15] [Impact Index Per Article: 5.0] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Figures] [Subscribe] [Scholar Register] [Received: 11/19/2021] [Revised: 02/14/2022] [Accepted: 02/22/2022] [Indexed: 02/07/2023]

Wei LY, Zhang JK, Zheng L, Chen Y. The functional role of sulforaphane in intestinal inflammation: a review. Food Funct 2021;13:514-529. [PMID: 34935814 DOI: 10.1039/d1fo03398k] [Citation(s) in RCA: 27] [Impact Index Per Article: 6.8] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 12/18/2022]

Yan J, Ouyang J, Isnard S, Zhou X, Harypursat V, Routy JP, Chen Y. Alcohol Use and Abuse Conspires With HIV Infection to Aggravate Intestinal Dysbiosis and Increase Microbial Translocation in People Living With HIV: A Review. Front Immunol 2021;12:741658. [PMID: 34975838 PMCID: PMC8718428 DOI: 10.3389/fimmu.2021.741658] [Citation(s) in RCA: 9] [Impact Index Per Article: 2.3] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 07/16/2021] [Accepted: 11/30/2021] [Indexed: 12/12/2022] Open

Wang H, Ye C, Wu Y, Yang P, Chen C, Liu Z, Wang X. Exosomes in Inflammatory Bowel Disease: What Have We Learned So Far? Curr Drug Targets 2021;21:1448-1455. [PMID: 32342815 DOI: 10.2174/1389450121666200428102330] [Citation(s) in RCA: 5] [Impact Index Per Article: 1.3] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 01/28/2020] [Revised: 02/17/2020] [Accepted: 02/17/2020] [Indexed: 01/06/2023]

Pinson MR, Chung DD, Adams AM, Scopice C, Payne EA, Sivakumar M, Miranda RC. Extracellular Vesicles in Premature Aging and Diseases in Adulthood Due to Developmental Exposures. Aging Dis 2021;12:1516-1535. [PMID: 34527425 PMCID: PMC8407878 DOI: 10.14336/ad.2021.0322] [Citation(s) in RCA: 7] [Impact Index Per Article: 1.8] [Reference Citation Analysis] [Abstract] [Key Words] [Grants] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 01/11/2021] [Accepted: 03/22/2021] [Indexed: 12/12/2022] Open

Campana L, Esser H, Huch M, Forbes S. Liver regeneration and inflammation: from fundamental science to clinical applications. Nat Rev Mol Cell Biol 2021;22:608-624. [PMID: 34079104 DOI: 10.1038/s41580-021-00373-7] [Citation(s) in RCA: 153] [Impact Index Per Article: 38.3] [Reference Citation Analysis] [Abstract] [MESH Headings] [Grants] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Accepted: 04/20/2021] [Indexed: 02/05/2023]

Silva CBP, Elias-Oliveira J, McCarthy CG, Wenceslau CF, Carlos D, Tostes RC. Ethanol: striking the cardiovascular system by harming the gut microbiota. Am J Physiol Heart Circ Physiol 2021;321:H275-H291. [PMID: 34142885 DOI: 10.1152/ajpheart.00225.2021] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 11/22/2022]

Alberca RW, Rigato PO, Ramos YÁL, Teixeira FME, Branco ACC, Fernandes IG, Pietrobon AJ, Duarte AJDS, Aoki V, Orfali RL, Sato MN. Clinical Characteristics and Survival Analysis in Frequent Alcohol Consumers With COVID-19. Front Nutr 2021;8:689296. [PMID: 34150832 PMCID: PMC8206498 DOI: 10.3389/fnut.2021.689296] [Citation(s) in RCA: 7] [Impact Index Per Article: 1.8] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 03/31/2021] [Accepted: 04/29/2021] [Indexed: 12/15/2022] Open

Affiliation(s)

Ricardo Wesley Alberca Laboratorio de Dermatologia e Imunodeficiencias (LIM-56), Departamento de Dermatologia, Faculdade de Medicina FMUSP, Instituto de Medicina Tropica, Universidade de São Paulo, São Paulo, Brazil
Paula Ordonhez Rigato Technical Division of Medical Biology, Immunology Center, Adolfo Lutz Institute, São Paulo, Brazil
Yasmim Álefe Leuzzi Ramos Laboratorio de Dermatologia e Imunodeficiencias (LIM-56), Departamento de Dermatologia, Faculdade de Medicina FMUSP, Instituto de Medicina Tropica, Universidade de São Paulo, São Paulo, Brazil
Franciane Mouradian Emidio Teixeira Laboratorio de Dermatologia e Imunodeficiencias (LIM-56), Departamento de Dermatologia, Faculdade de Medicina FMUSP, Instituto de Medicina Tropica, Universidade de São Paulo, São Paulo, Brazil.,Department of Immunology, Institute of Biomedical Sciences, University of São Paulo, São Paulo, Brazil
Anna Cláudia Calvielli Branco Laboratorio de Dermatologia e Imunodeficiencias (LIM-56), Departamento de Dermatologia, Faculdade de Medicina FMUSP, Instituto de Medicina Tropica, Universidade de São Paulo, São Paulo, Brazil.,Department of Immunology, Institute of Biomedical Sciences, University of São Paulo, São Paulo, Brazil
Iara Grigoletto Fernandes Laboratorio de Dermatologia e Imunodeficiencias (LIM-56), Departamento de Dermatologia, Faculdade de Medicina FMUSP, Instituto de Medicina Tropica, Universidade de São Paulo, São Paulo, Brazil
Anna Julia Pietrobon Laboratorio de Dermatologia e Imunodeficiencias (LIM-56), Departamento de Dermatologia, Faculdade de Medicina FMUSP, Instituto de Medicina Tropica, Universidade de São Paulo, São Paulo, Brazil.,Department of Immunology, Institute of Biomedical Sciences, University of São Paulo, São Paulo, Brazil
Alberto Jose da Silva Duarte Laboratorio de Dermatologia e Imunodeficiencias (LIM-56), Departamento de Dermatologia, Faculdade de Medicina FMUSP, Instituto de Medicina Tropica, Universidade de São Paulo, São Paulo, Brazil
Valeria Aoki Laboratorio de Dermatologia e Imunodeficiencias (LIM-56), Departamento de Dermatologia, Faculdade de Medicina FMUSP, Instituto de Medicina Tropica, Universidade de São Paulo, São Paulo, Brazil
Raquel Leão Orfali Laboratorio de Dermatologia e Imunodeficiencias (LIM-56), Departamento de Dermatologia, Faculdade de Medicina FMUSP, Instituto de Medicina Tropica, Universidade de São Paulo, São Paulo, Brazil
Maria Notomi Sato Laboratorio de Dermatologia e Imunodeficiencias (LIM-56), Departamento de Dermatologia, Faculdade de Medicina FMUSP, Instituto de Medicina Tropica, Universidade de São Paulo, São Paulo, Brazil

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Liu SY, Tsai IT, Hsu YC. Alcohol-Related Liver Disease: Basic Mechanisms and Clinical Perspectives. Int J Mol Sci 2021;22:5170. [PMID: 34068269 PMCID: PMC8153142 DOI: 10.3390/ijms22105170] [Citation(s) in RCA: 67] [Impact Index Per Article: 16.8] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Download PDF] [Journal Information] [Subscribe] [Scholar Register] [Received: 04/17/2021] [Revised: 05/07/2021] [Accepted: 05/12/2021] [Indexed: 12/12/2022] Open

Yang J, Syed F, Xia Y, Sanyal A, Shah V, Chalasani N, Zheng X, Yu Q, Lou Y, Li W. Blood Biomarkers of Intestinal Epithelium Damage Regenerating Islet-derived Protein 3α and Trefoil Factor 3 Are Persistently Elevated in Patients with Alcoholic Hepatitis. Alcohol Clin Exp Res 2021;45:720-731. [PMID: 33587293 PMCID: PMC8076084 DOI: 10.1111/acer.14579] [Citation(s) in RCA: 5] [Impact Index Per Article: 1.3] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Grants] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 08/25/2020] [Accepted: 02/11/2021] [Indexed: 11/27/2022]

Abstract

BACKGROUND

Heavy alcohol consumption disrupts gut epithelial integrity, leading to increased permeability of the gastrointestinal tract and subsequent translocation of microbes. Regenerating islet-derived protein 3α (REG3α) and Trefoil factor 3 (TFF3) are mainly secreted to the gut lumen by Paneth and Goblet cells, respectively, and are functionally linked to gut barrier integrity. Circulating levels of REG3α and TFF3 have been identified as biomarkers for gut damage in several human diseases. We examined whether plasma levels of REG3α and TFF3 were dysregulated and correlated with conventional markers of microbial translocation (MT) and pro-inflammatory mediators in heavy drinkers with and without alcoholic hepatitis (AH).

METHODS

Cross-sectional and longitudinal studies were performed to monitor plasma levels of REG3α and TFF3 in 79 AH patients, 66 heavy drinkers without liver disease (HDC), and 46 healthy controls (HC) at enrollment and at 6- and 12-month follow-ups. Spearman correlation was used to measure the relationships of REG3α and TFF3 levels with MT, disease severity, inflammation, and effects of abstinence from alcohol.

RESULTS

At enrollment, AH patients had significantly higher levels of REG3α and TFF3 than HDC and HC. The elevated REG3α levels were positively correlated with the 30-day fatality rate. Plasma levels of REG3α and TFF3 in AH patients differentially correlated with conventional MT markers (sCD14, sCD163, and LBP) and several highly up-regulated inflammatory cytokines/chemokines/growth factors. At follow-ups, although REG3α and TFF3 levels were decreased in AH patients with alcohol abstinence, they did not fully return to baseline levels.

CONCLUSIONS

Circulating levels of REG3α and TFF3 were highly elevated in AH patients and differentially correlated with AH disease severity, MT, and inflammation, thereby serving as potential biomarkers of MT and gut epithelial damage in AH patients.

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Huang W, Kong D. The intestinal microbiota as a therapeutic target in the treatment of NAFLD and ALD. Biomed Pharmacother 2021;135:111235. [DOI: 10.1016/j.biopha.2021.111235] [Citation(s) in RCA: 5] [Impact Index Per Article: 1.3] [Reference Citation Analysis] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 10/29/2020] [Revised: 12/27/2020] [Accepted: 12/31/2020] [Indexed: 02/08/2023] Open

Morris NL, Choudhry MA. Maintenance of gut barrier integrity after injury: Trust your gut microRNAs. J Leukoc Biol 2021;110:979-986. [PMID: 33577717 DOI: 10.1002/jlb.3ru0120-090rr] [Citation(s) in RCA: 1] [Impact Index Per Article: 0.3] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 01/31/2020] [Revised: 01/20/2021] [Accepted: 01/21/2021] [Indexed: 12/11/2022] Open

García-Baos A, Alegre-Zurano L, Cantacorps L, Martín-Sánchez A, Valverde O. Role of cannabinoids in alcohol-induced neuroinflammation. Prog Neuropsychopharmacol Biol Psychiatry 2021;104:110054. [PMID: 32758518 DOI: 10.1016/j.pnpbp.2020.110054] [Citation(s) in RCA: 11] [Impact Index Per Article: 2.8] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 04/30/2020] [Revised: 07/13/2020] [Accepted: 07/29/2020] [Indexed: 02/06/2023]

Ramos-Lopez O, Milagro FI, Riezu-Boj JI, Martinez JA. Epigenetic signatures underlying inflammation: an interplay of nutrition, physical activity, metabolic diseases, and environmental factors for personalized nutrition. Inflamm Res 2021;70:29-49. [PMID: 33231704 PMCID: PMC7684853 DOI: 10.1007/s00011-020-01425-y] [Citation(s) in RCA: 79] [Impact Index Per Article: 19.8] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 09/08/2020] [Revised: 10/26/2020] [Accepted: 11/12/2020] [Indexed: 12/12/2022] Open

Kang EA, Choi HI, Hong SW, Kang S, Jegal HY, Choi EW, Park BS, Kim JS. Extracellular Vesicles Derived from Kefir Grain Lactobacillus Ameliorate Intestinal Inflammation via Regulation of Proinflammatory Pathway and Tight Junction Integrity. Biomedicines 2020;8:biomedicines8110522. [PMID: 33233771 PMCID: PMC7709018 DOI: 10.3390/biomedicines8110522] [Citation(s) in RCA: 42] [Impact Index Per Article: 8.4] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 10/13/2020] [Revised: 11/17/2020] [Accepted: 11/18/2020] [Indexed: 12/19/2022] Open

The Gut Microbiota: How Does It Influence the Development and Progression of Liver Diseases. Biomedicines 2020;8:biomedicines8110501. [PMID: 33207562 PMCID: PMC7697996 DOI: 10.3390/biomedicines8110501] [Citation(s) in RCA: 23] [Impact Index Per Article: 4.6] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 10/13/2020] [Revised: 11/06/2020] [Accepted: 11/13/2020] [Indexed: 02/07/2023] Open

Ganguly K, Kishore U, Madan T. Interplay between C-type lectin receptors and microRNAs in cellular homeostasis and immune response. FEBS J 2020;288:4210-4229. [PMID: 33085815 DOI: 10.1111/febs.15603] [Citation(s) in RCA: 7] [Impact Index Per Article: 1.4] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 07/27/2020] [Revised: 09/18/2020] [Accepted: 10/15/2020] [Indexed: 12/14/2022]

Skinner C, Thompson AJ, Thursz MR, Marchesi JR, Vergis N. Intestinal permeability and bacterial translocation in patients with liver disease, focusing on alcoholic aetiology: methods of assessment and therapeutic intervention. Therap Adv Gastroenterol 2020;13:1756284820942616. [PMID: 33149761 PMCID: PMC7580143 DOI: 10.1177/1756284820942616] [Citation(s) in RCA: 20] [Impact Index Per Article: 4.0] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 03/31/2020] [Accepted: 06/25/2020] [Indexed: 02/04/2023] Open

Tornai D, Szabo G. Emerging medical therapies for severe alcoholic hepatitis. Clin Mol Hepatol 2020;26:686-696. [PMID: 32981291 PMCID: PMC7641578 DOI: 10.3350/cmh.2020.0145] [Citation(s) in RCA: 8] [Impact Index Per Article: 1.6] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 07/02/2020] [Accepted: 08/28/2020] [Indexed: 12/12/2022] Open

Wu G, Win S, Than TA, Chen P, Kaplowitz N. Gut Microbiota and Liver Injury (I)-Acute Liver Injury. ADVANCES IN EXPERIMENTAL MEDICINE AND BIOLOGY 2020;1238:23-37. [PMID: 32323178 DOI: 10.1007/978-981-15-2385-4_3] [Citation(s) in RCA: 2] [Impact Index Per Article: 0.4] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Subscribe] [Scholar Register] [Indexed: 12/13/2022]

Steve M D, Lindsey B C, Byung Soo Y, Parth J P, David A J. Microbiome and Gastroesophageal Disease: Pathogenesis and Implications for Therapy. ACTA ACUST UNITED AC 2020. [DOI: 10.29328/journal.acgh.1001018] [Citation(s) in RCA: 1] [Impact Index Per Article: 0.2] [Reference Citation Analysis] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 01/05/2023]

Fu X, He HD, Li CJ, Li N, Jiang SY, Ge HW, Wang R, Wang XL. MicroRNA-155 deficiency attenuates inflammation and oxidative stress in experimental autoimmune prostatitis in a TLR4-dependent manner. Kaohsiung J Med Sci 2020;36:712-720. [PMID: 32436368 DOI: 10.1002/kjm2.12229] [Citation(s) in RCA: 5] [Impact Index Per Article: 1.0] [Reference Citation Analysis] [Abstract] [Key Words] [Journal Information] [Subscribe] [Scholar Register] [Received: 12/27/2019] [Revised: 03/03/2020] [Accepted: 04/19/2020] [Indexed: 12/26/2022] Open

Abstract

To explore the mechanism of microRNA-155 (miR-155) deficiency, protecting against experimental autoimmune prostatitis (EAP) in a toll-like receptor 4 (TLR4)-dependent manner. After wild-type (WT) and miR-155^-/- mice were injected with complete Freund's adjuvant and prostate antigen to establish EAP model, half were randomly selected for injection with lipopolysaccharide (LPS, a TLR4 ligand). The following experiments were then performed: von Frey filaments, hematoxylin-eosin (HE) staining, real time quantitative polymerase chain reaction (qRT-PCR), Western blotting, and enzyme-linked immunosorbent assay (ELISA). And the activities of superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) and the level of Malondialdehyde (MDA) were detected by corresponding kits.miR-155^-/- mice with prostatitis exhibited the attenuated pelvic tactile allodynia/hyperalgesia and the suppressed TLR4/nuclear factor-kappa B (NF-κB) pathway as compared with the WT mice with prostatitis. In addition, LPS enhanced the upregulation of miR-155 and the activation of the TLR4/NF-κB pathway in the prostatic tissues of WT mice with EAP. Furthermore, prostatitis mice had aggravated inflammation scores accompanying the increased interleukin (IL)-1β, tumor necrosis factor-α, IL-6, interferon-γ, IL-12, and MDA in prostatic tissues with the decreased IL-10, SOD and GSH-Px, and the unaltered IL-4. Compared with the mice from the WT + EAP group and the miR-155^-/- + EAP + LPS group, mice from the miR-155^-/- + EAP group had decreased inflammation and oxidative stress. miR-155 deficiency ameliorated pelvic tactile allodynia/hyperalgesia in EAP mice and improved inflammation and oxidative stress in prostatic tissues in a TLR4-dependent manner involving NF-κB activation, thereby exerting a therapeutic effect in chronic prostatitis treatment.

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miR-155 Knockdown Protects against Cerebral Ischemia and Reperfusion Injury by Targeting MafB. BIOMED RESEARCH INTERNATIONAL 2020;2020:6458204. [PMID: 32090104 PMCID: PMC6996700 DOI: 10.1155/2020/6458204] [Citation(s) in RCA: 17] [Impact Index Per Article: 3.4] [Reference Citation Analysis] [Abstract] [Track Full Text] [Download PDF] [Figures] [Subscribe] [Scholar Register] [Received: 09/26/2019] [Accepted: 11/28/2019] [Indexed: 01/30/2023]

Abstract

Background

Studies have elucidated that the variable expression levels of miRNAs influence the inflammatory process in ischemic stroke. Nevertheless, the impact and potential mechanism of miR-155 in cerebral ischemia-reperfusion injury (CIRI) keep to be incompletely known.

Methods

The levels of miR-155 and MafB were determined via qRT-PCR, western blot, or immunohistochemistry assays in plasma of patients with CIRI, oxygen glucose deprivation/reoxygenation (OGD/R) induced SH-SY5Y cells, and mouse models with middle cerebral artery occlusion (MCAO). The association between miR-155 and MafB was validated via dual-luciferase reporter and western blot assays. Cell viability, apoptosis, invasion, and migration were evaluated through MTT, flow cytometry, Transwell and wound healing assays. Infarction volume was measured in MCAO mouse brain tissues by TTC assay. The expression of inflammatory mediators was measured by ELISA in cells and brain tissues.

Results

miR-155 level was upregulated whereas MafB was downregulated in the plasma of patients with CIRI, OGD/R-induced SH-SY5Y cells, also as mouse models with MCAO injury. Mechanistically, miR-155 directly targeted 3'UTR of MafB and restrained MafB expression in OGD/R injury SH-SY5Y cells. Downregulation of miR-155 attenuated OGD/R-induced injury through increasing proliferation, inhibiting apoptosis, enhancing invasion and migration abilities, and constraining the expression of inflammatory mediators (IL-1β, IL-6, and TNF-α) and inflammatory enzymes (iNOS and COX-2) in SH-SY5Y cells following OGD/R, while MafB inhibition reversed the protective effects. In vivo, downregulating miR-155 reduced the infarction volume in the MACO mouse brain. Furthermore, miR-155 knockdown inhibited the IL-1β, IL-6, and TNF-α) and inflammatory enzymes (iNOS and COX-2) in SH-SY5Y cells following OGD/R, while MafB inhibition reversed the protective effects.

Conclusion

Our results suggest that miR-155 knockdown alleviated ischemia-reperfusion injury by targeting MafB to improve the neurological function and inhibit inflammation response, highlighting a novel therapeutic strategist for CIRI.

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Bataller R, Cabezas J, Aller R, Ventura-Cots M, Abad J, Albillos A, Altamirano J, Arias-Loste MT, Bañares R, Caballería J, Caballería L, Carrión JA, Diago M, Fernández Rodríguez C, Gallego R, García-Cortes M, García-Monzón C, Genescà J, Ginés P, Hernandez-Guerra M, Jorquera F, Lligoña A, Molina E, Pareja MJ, Planas R, Tomé S, Salmerón J, Romero-Gómez M. Alcohol-related liver disease. Clinical practice guidelines. Consensus document sponsored by AEEH. GASTROENTEROLOGIA Y HEPATOLOGIA 2019;42:657-676. [PMID: 31771785 DOI: 10.1016/j.gastrohep.2019.09.006] [Citation(s) in RCA: 8] [Impact Index Per Article: 1.3] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Subscribe] [Scholar Register] [Received: 08/31/2019] [Accepted: 09/02/2019] [Indexed: 02/07/2023]

Affiliation(s)

Ramón Bataller Department of Medicine, Division of Gastroenterology, Hepatology and Nutrition, Center for Liver Diseases, University of Pittsburgh Medical Center, Pittsburgh, PA, Estados Unidos.
Joaquín Cabezas Servicio de Aparato Digestivo, Hospital Universitario Marqués de Valdecilla, Instituto de investigación Sanitaria Valdecilla (IDIVAL), Santander, Cantabria, España; Centro de Investigación Biomédica en Red de Enfermedades Hepáticas y Digestivas (CIBERehd), Instituto de Salud Carlos III, Madrid, España
Rocío Aller Servicio de Gastroenterología, Hospital Clínico Universitario de Valladolid, Valladolid, España; Facultad de Medicina, Universidad de Valladolid, Valladolid, España; Centro de Investigación de Endocrinología y Nutrición, Facultad de Medicina de Valladolid, Valladolid, España
Meritxell Ventura-Cots Department of Medicine, Division of Gastroenterology, Hepatology and Nutrition, Center for Liver Diseases, University of Pittsburgh Medical Center, Pittsburgh, PA, Estados Unidos; Centro de Investigación Biomédica en Red de Enfermedades Hepáticas y Digestivas (CIBERehd), Instituto de Salud Carlos III, Madrid, España
Javier Abad Servicio de Gastroenterología y Hepatología, Hospital Puerta de Hierro, Madrid, España
Agustín Albillos Centro de Investigación Biomédica en Red de Enfermedades Hepáticas y Digestivas (CIBERehd), Instituto de Salud Carlos III, Madrid, España; Servicio de Gastroenterología y Hepatología, Hospital Universitario Ramón y Cajal, Universidad de Alcalá, Instituto Ramón y Cajal de Investigación Sanitaria (IRYCIS), Madrid, España
José Altamirano Deparmento de Medicina Interna, Hospital Quironsalud, Barcelona, España
María Teresa Arias-Loste Servicio de Aparato Digestivo, Hospital Universitario Marqués de Valdecilla, Instituto de investigación Sanitaria Valdecilla (IDIVAL), Santander, Cantabria, España; Centro de Investigación Biomédica en Red de Enfermedades Hepáticas y Digestivas (CIBERehd), Instituto de Salud Carlos III, Madrid, España
Rafael Bañares Centro de Investigación Biomédica en Red de Enfermedades Hepáticas y Digestivas (CIBERehd), Instituto de Salud Carlos III, Madrid, España; Servicio de Gastroenterología y Hepatología, Hospital Gregorio Marañón, Madrid, España
Juan Caballería Centro de Investigación Biomédica en Red de Enfermedades Hepáticas y Digestivas (CIBERehd), Instituto de Salud Carlos III, Madrid, España; Unidad de Hepatología, Hospital Clínic, IDIBAPS, Barcelona, España
Llorenç Caballería Unidad de Apoyo a la Investigación de la Atención Primaria en la Metropolitana Norte, Barcelona, España
José Antonio Carrión Unidad Hepática, Servicio de Digestivo, Hospital del Mar, Barcelona, España
Moisés Diago Servicio de Aparato Digestivo, Hospital General de Valencia, Valencia, España
Conrado Fernández Rodríguez Servicio de Gastroenterología, Hospital Universitario Fundación Alcorcón. Facultad de Medicina, Universidad Rey Juan Carlos, Alcorcón, Madrid, España
Rocío Gallego Centro de Investigación Biomédica en Red de Enfermedades Hepáticas y Digestivas (CIBERehd), Instituto de Salud Carlos III, Madrid, España; UGC Aparato Digestivo, Instituto de Biomedicina de Sevilla. Hospital Universitario Virgen del Rocío, Universidad de Sevilla, Sevilla, España
Miren García-Cortes UGC Aparato Digestivo, Hospital Virgen de la Victoria, Málaga, España
Carmelo García-Monzón Servicio de Medicina Interna, Hospital Universitario Santa Cristina, Madrid, España
Joan Genescà Centro de Investigación Biomédica en Red de Enfermedades Hepáticas y Digestivas (CIBERehd), Instituto de Salud Carlos III, Madrid, España; Servicio de Medicina Interna-Hepatología, Hospital Universitario Vall d'Hebron, Institut de Recerca Vall d'Hebron (VHIR), Universitat Autònoma de Barcelona, Barcelona, España
Pere Ginés Centro de Investigación Biomédica en Red de Enfermedades Hepáticas y Digestivas (CIBERehd), Instituto de Salud Carlos III, Madrid, España; Unidad de Apoyo a la Investigación de la Atención Primaria en la Metropolitana Norte, Barcelona, España
Manuel Hernandez-Guerra Servicio de Digestivo, Hospital Universitario de Canarias, Tenerife, Islas Canarias, España
Francisco Jorquera Centro de Investigación Biomédica en Red de Enfermedades Hepáticas y Digestivas (CIBERehd), Instituto de Salud Carlos III, Madrid, España; Servicio de Aparato Digestivo, Complejo Asistencial Universitario de León, IBIOMED, León, España
Anna Lligoña Unidad de Alcohologia, Departamento de Psiquiatría, Hospital Clínic. Barcelona, España
Esther Molina Unidad de Hepatología, Servicio de Aparato Digestivo, Hospital Clínico-Xerencia de Xestión Integrada de Santiago de Compostela, Santiago de Compostela, La Coruña, España
María Jesús Pareja UGC de Aparato Digestivo, Hospital Juan Ramón Jiménez, Huelva, España
Ramón Planas Centro de Investigación Biomédica en Red de Enfermedades Hepáticas y Digestivas (CIBERehd), Instituto de Salud Carlos III, Madrid, España; Departamento de Hepatología, Hospital Germans Trias i Pujol, Badalona, Barcelona, España
Santiago Tomé Unidad de Trasplante Hepático, Hospital Clínico Universitario, Santiago de Compostela, La Coruña, España
Javier Salmerón UGC de Aparato Digestivo, Hospital San Cecilio, Granada, España
Manuel Romero-Gómez Centro de Investigación Biomédica en Red de Enfermedades Hepáticas y Digestivas (CIBERehd), Instituto de Salud Carlos III, Madrid, España; UGC Aparato Digestivo, Instituto de Biomedicina de Sevilla. Hospital Universitario Virgen del Rocío, Universidad de Sevilla, Sevilla, España

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Zhang KK, Yu SS, Li GY, He L, Liang XQ. miR-135a deficiency inhibits the AR42J cells damage in cerulein-induced acute pancreatitis through targeting FAM129A. Pflugers Arch 2019;471:1519-1527. [PMID: 31729558 DOI: 10.1007/s00424-019-02329-5] [Citation(s) in RCA: 2] [Impact Index Per Article: 0.3] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 04/29/2019] [Revised: 10/16/2019] [Accepted: 11/06/2019] [Indexed: 01/27/2023]

Inoue T, Nakayama J, Moriya K, Kawaratani H, Momoda R, Ito K, Iio E, Nojiri S, Fujiwara K, Yoneda M, Yoshiji H, Tanaka Y. Gut Dysbiosis Associated With Hepatitis C Virus Infection. Clin Infect Dis 2019;67:869-877. [PMID: 29718124 DOI: 10.1093/cid/ciy205] [Citation(s) in RCA: 124] [Impact Index Per Article: 20.7] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 07/22/2017] [Accepted: 03/06/2018] [Indexed: 12/12/2022] Open

Simbrunner B, Mandorfer M, Trauner M, Reiberger T. Gut-liver axis signaling in portal hypertension. World J Gastroenterol 2019;25:5897-5917. [PMID: 31660028 PMCID: PMC6815800 DOI: 10.3748/wjg.v25.i39.5897] [Citation(s) in RCA: 76] [Impact Index Per Article: 12.7] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Download PDF] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 06/03/2019] [Revised: 08/15/2019] [Accepted: 09/28/2019] [Indexed: 02/06/2023] Open

Alcohol-induced IL-17A production in Paneth cells amplifies endoplasmic reticulum stress, apoptosis, and inflammasome-IL-18 activation in the proximal small intestine in mice. Mucosal Immunol 2019;12:930-944. [PMID: 31105269 PMCID: PMC6599481 DOI: 10.1038/s41385-019-0170-4] [Citation(s) in RCA: 28] [Impact Index Per Article: 4.7] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 03/16/2018] [Revised: 04/05/2019] [Accepted: 04/13/2019] [Indexed: 02/06/2023]

Zhang H, Wang L, Li C, Yu Y, Yi Y, Wang J, Chen D. Exosome-Induced Regulation in Inflammatory Bowel Disease. Front Immunol 2019;10:1464. [PMID: 31316512 PMCID: PMC6611439 DOI: 10.3389/fimmu.2019.01464] [Citation(s) in RCA: 112] [Impact Index Per Article: 18.7] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 08/08/2018] [Accepted: 06/10/2019] [Indexed: 12/21/2022] Open

Feng R, Chen JH, Liu CH, Xia FB, Xiao Z, Zhang X, Wan JB. A combination of Pueraria lobata and Silybum marianum protects against alcoholic liver disease in mice. PHYTOMEDICINE : INTERNATIONAL JOURNAL OF PHYTOTHERAPY AND PHYTOPHARMACOLOGY 2019;58:152824. [PMID: 30836218 DOI: 10.1016/j.phymed.2019.152824] [Citation(s) in RCA: 18] [Impact Index Per Article: 3.0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Subscribe] [Scholar Register] [Received: 10/10/2018] [Revised: 01/03/2019] [Accepted: 01/08/2019] [Indexed: 05/19/2023]

Abstract

BACKGROUND

Excess alcohol exposure leads to alcoholic liver disease (ALD). Pueraria lobata (PUE) and Silybum marianum (SIL) are two well-known hepatoprotective herbal remedies with various activities. The possible effect of combination of PUE and SIL on ALD has not been elucidated yet.

PURPOSE

We aimed to demonstrate that the combination of PUE and SIL prevents against alcoholic liver injury in mice using a model of chronic-plus-single-binge ethanol feeding.

STUDY DESIGN

Male C57BL/6 mice were randomly divided into five groups (n = 8-10), namely the control group (CON), ethanol-induced liver injury group (ETH), 150 mg/kg PUE treated group (PUE), 60 mg/kg SIL treated group (SIL), 210 mg/kg PUE+SIL treatment group (PUE+SIL). Except control group, all animals were fed a modified Lieber-DeCarli ethanol liquid diet for 10 days. While, control group received Lieber-DeCarli control diet containing isocaloric maltose dextrin substituted for ethanol. On day 11, the mice orally received a single dose of 31.5% (v/v) ethanol (5 g/kg BW) or an isocaloric maltose solution.

RESULTS

Ethanol exposure caused liver injury, as demonstrated by remarkably increased plasma parameters, histopathological changes, the increased lipid accumulation, oxidative stress and inflammation in liver. These alterations were ameliorated by the treatments of PUE, SIL and PUE+SIL. While, the PUE+SIL treatment showed the most effective protection, which was associated with reducing alcohol-induced hepatic steatosis via upregulating LKB1/AMPK/ACC signaling, and inhibiting hepatic inflammation via LPS-triggered TLR4-mediated NF-κB signaling pathway. Our results also indicated that the hepatoprotective effects of SIL+PUE might mainly attribute to the protection of SIL and PUE alone in alcohol-induced hepatic steatosis and hepatic inflammation, respectively.

CONCLUSION

These findings also suggest that the combination of PUE and SIL has a potential to be developed as a functional food for the management of ALD.

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Wang W, Xu Y, Jiang C, Gao Y. Advances in the treatment of severe alcoholic hepatitis. Curr Med Res Opin 2019;35:261-273. [PMID: 29781336 DOI: 10.1080/03007995.2018.1479247] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 10/16/2022]

Singal AK, Shah VH. Current trials and novel therapeutic targets for alcoholic hepatitis. J Hepatol 2019;70:305-313. [PMID: 30658731 DOI: 10.1016/j.jhep.2018.10.026] [Citation(s) in RCA: 90] [Impact Index Per Article: 15.0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 10/04/2018] [Accepted: 10/24/2018] [Indexed: 12/12/2022]

Yang Y, Ai G, Wang M. Alcoholic liver disease and intestinal microecology. Shijie Huaren Xiaohua Zazhi 2019;27:43-49. [DOI: 10.11569/wcjd.v27.i1.43] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 02/06/2023] Open