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Song D, Zhao X, Zhang Y, Wang M, Tang H, Fang J, Song Z, Ma Q, Geng J. The amelioration effect of sesamoside on inflammatory response in septic shock. BMC Immunol 2025; 26:15. [PMID: 40050706 PMCID: PMC11884088 DOI: 10.1186/s12865-025-00695-7] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Grants] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 11/19/2024] [Accepted: 02/26/2025] [Indexed: 03/10/2025] Open
Abstract
Sepsis shock is caused by a systemic infection characterized by circulatory disorders and metabolic abnormalities. Microorganisms or their toxins enter the bloodstream, releasing inflammatory mediators and triggering systemic inflammatory reactions, leading to multiple organ dysfunction and even failure. To explore new treatment methods, we studied the improvement effect of sesamoside on the inflammatory response in septic shock. We performed in vitro experiments and animal models. We found that sesamoside reduced inflammatory cytokines such as TNF-α, IL-6, IL-1β, iNOS, and NO. Sesamoside inhibited the LPS-induced phosphorylation of ERK and JNK and downregulated the expression of NLRP3, reducing the systemic inflammatory response. In addition, sesamoside reduces multi-organ injuries in LPS-induced septic shock and restricts the nuclear localization of P65 to regulate the immune response, enhance immune function, and help restore cell metabolism and organ function. This study reveals the improved effect of sesamoside on inflammatory response in septic shock, providing new ideas and methods for treating septic shock. Future research will explore the mechanism of action of sesamoside and its clinical application value in the treatment of septic shock. Clinical trial number: Not applicable.
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Affiliation(s)
- Dan Song
- Key Laboratory for Molecular Genetic Mechanisms and Intervention Research on High Altitude Disease of Tibet Autonomous Region, School of Medicine, Xizang Minzu University, Xianyang, Shaanxi, 712082, China
| | - Xinjie Zhao
- Key Laboratory for Molecular Genetic Mechanisms and Intervention Research on High Altitude Disease of Tibet Autonomous Region, School of Medicine, Xizang Minzu University, Xianyang, Shaanxi, 712082, China
| | - Yanru Zhang
- Key Laboratory for Molecular Genetic Mechanisms and Intervention Research on High Altitude Disease of Tibet Autonomous Region, School of Medicine, Xizang Minzu University, Xianyang, Shaanxi, 712082, China
| | - Mengjie Wang
- Key Laboratory for Molecular Genetic Mechanisms and Intervention Research on High Altitude Disease of Tibet Autonomous Region, School of Medicine, Xizang Minzu University, Xianyang, Shaanxi, 712082, China
| | - Haojie Tang
- Key Laboratory for Molecular Genetic Mechanisms and Intervention Research on High Altitude Disease of Tibet Autonomous Region, School of Medicine, Xizang Minzu University, Xianyang, Shaanxi, 712082, China
| | - Jing Fang
- Key Laboratory for Molecular Genetic Mechanisms and Intervention Research on High Altitude Disease of Tibet Autonomous Region, School of Medicine, Xizang Minzu University, Xianyang, Shaanxi, 712082, China
| | - Zhuoyang Song
- Key Laboratory for Molecular Genetic Mechanisms and Intervention Research on High Altitude Disease of Tibet Autonomous Region, School of Medicine, Xizang Minzu University, Xianyang, Shaanxi, 712082, China
| | - Qingyang Ma
- Key Laboratory for Molecular Genetic Mechanisms and Intervention Research on High Altitude Disease of Tibet Autonomous Region, School of Medicine, Xizang Minzu University, Xianyang, Shaanxi, 712082, China
| | - Jing Geng
- National and Local Joint Engineering Research Center of Biodiagnosis and Biotherapy, The Second Affiliated Hospital of Xi'an Jiaotong University, Xi'an, Shaanxi, 710004, China.
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Yin K, Yang J, Wang F, Wang Z, Xiang P, Xie X, Sun J, He X, Zhang X. A preliminary study of the chemical composition and bioactivity of Bombax ceiba L. flower and its potential mechanism in treating type 2 diabetes mellitus using ultra-performance liquid chromatography quadrupole-time-flight mass spectrometry and network pharmacology analysis. Front Nutr 2022; 9:1018733. [PMID: 36313078 PMCID: PMC9608341 DOI: 10.3389/fnut.2022.1018733] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 08/13/2022] [Accepted: 09/29/2022] [Indexed: 12/03/2022] Open
Abstract
This study aimed to preliminary investigate the phytochemistry, bioactivity, hypoglycemic potential, and mechanism of action of Bombax ceiba L. flower (BCF), a wild edible and food plant in China. By using methanol extraction and liquid-liquid extraction, the crude extract (CE) of BCF and its petroleum ether (PE), dichloromethane (DCM), ethyl acetate (EtOAc), n-butanol (n-BuOH), and aqueous (AQ) fractions were obtained, and their chemical components and biological activities were evaluated. Further high-performance liquid chromatography (HPLC) analysis was carried out to identify and quantify the active constituents of BFC and its five fractions, and the phytochemical composition of the best-performing fraction was then analyzed by ultra-performance liquid chromatography quadrupole-time-flight mass spectrometry (UPLC/Q-TOF-MS). Finally, a network pharmacology strategy based on the chemical profile of this fraction was applied to speculate its main hypoglycemic mechanism. Results revealed the excellent biological activities of BCF, especially the EtOAc fraction. In addition to the highest total flavonoid content (TFC) (367.72 μg RE/mg E) and total phenolics content (TPC) (47.97 μg GAE/mg E), EtOAc showed the strongest DPPH⋅ scavenging ability (IC50 value = 29.56 μg/mL), ABTS⋅+ scavenging ability (IC50 value = 84.60 μg/mL), and ferric reducing antioxidant power (FRAP) (889.62 μg FeSO4/mg E), which were stronger than the positive control BHT. EtOAc also exhibited the second-best α-glucosidase inhibitory capacity and second-best acetylcholinesterase (AChE) inhibitory capacity with the IC50 values of 2.85 and 3.27 mg/mL, respectively. Also, EtOAc inhibited HepG2, MCF-7, Raw264.7, and A549 cell with IC50 values of 1.08, 1.62, 0.77, and 0.87 mg/mL, which were the second or third strongest in all fractions. Additionally, HPLC analysis revealed significant differences in the compounds’ abundance between different fractions. Among them, EtOAc had the most detected compounds and the highest content. According to the results of UPLC/Q-TOF-MS, 38 compounds were identified in EtOAc, including 24 phenolic acids and 6 flavonoids. Network pharmacological analysis further confirmed 41 potential targets of EtOAc in the treatment of type 2 diabetes, and intracellular receptor signaling pathways, unsaturated fatty acid, and DNA transcription pathways were the most possible mechanisms. These findings suggested that BCF was worthwhile to be developed as an antioxidant and anti-diabetic food/drug.
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Affiliation(s)
- Kehong Yin
- Key Laboratory for Forest Resources Conservation and Utilization in the Southwest Mountains of China, Ministry of Education, College of Life Science, Southwest Forestry University, Kunming, China
| | - Jinmei Yang
- Key Laboratory for Forest Resources Conservation and Utilization in the Southwest Mountains of China, Ministry of Education, College of Life Science, Southwest Forestry University, Kunming, China
| | - Fang Wang
- Key Laboratory for Forest Resources Conservation and Utilization in the Southwest Mountains of China, Ministry of Education, College of Life Science, Southwest Forestry University, Kunming, China
| | - Zhenxing Wang
- Key Laboratory for Forest Resources Conservation and Utilization in the Southwest Mountains of China, Ministry of Education, College of Life Science, Southwest Forestry University, Kunming, China
| | - Ping Xiang
- Institute of Environmental Remediation and Human Health, Southwest Forestry University, Kunming, China
| | - Xing Xie
- National R&D Center for Freshwater Fish Processing, College of Health, Jiangxi Normal University, Nanchang, China
| | - Jian Sun
- Guangxi Key Laboratory of Fruits and Vegetables Storage-Processing Technology, Guangxi Academy of Agricultural Sciences, Nanning, China
| | - Xuemei He
- Guangxi Key Laboratory of Fruits and Vegetables Storage-Processing Technology, Guangxi Academy of Agricultural Sciences, Nanning, China,*Correspondence: Xuemei He,
| | - Xuechun Zhang
- Key Laboratory for Forest Resources Conservation and Utilization in the Southwest Mountains of China, Ministry of Education, College of Life Science, Southwest Forestry University, Kunming, China,Guangxi Key Laboratory of Fruits and Vegetables Storage-Processing Technology, Guangxi Academy of Agricultural Sciences, Nanning, China,Xuechun Zhang,
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Park MY, Ha SE, Kim HH, Bhosale PB, Abusaliya A, Jeong SH, Park JS, Heo JD, Kim GS. Scutellarein Inhibits LPS-Induced Inflammation through NF-κB/MAPKs Signaling Pathway in RAW264.7 Cells. MOLECULES (BASEL, SWITZERLAND) 2022; 27:molecules27123782. [PMID: 35744907 PMCID: PMC9227861 DOI: 10.3390/molecules27123782] [Citation(s) in RCA: 36] [Impact Index Per Article: 12.0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Download PDF] [Figures] [Subscribe] [Scholar Register] [Received: 05/23/2022] [Revised: 06/07/2022] [Accepted: 06/10/2022] [Indexed: 11/16/2022]
Abstract
Inflammation is a severe topic in the immune system and play a role as pro-inflammatory mediators. In response to such inflammatory substances, immune cells release cytokines such as tumor necrosis factor-α (TNF-α) and interleukin-1β (IL-1β). Lipopolysaccharide (LPS) is known as an endotoxin in the outer membrane of Gram-negative bacteria, and it catalyzes inflammation by stimulating the secretion of inflammatory-mediated cytokines such as cyclooxygenase-2 (COX-2) and inducible nitric oxide synthase (iNOS) by stimulated immune cells. Among the pathways involved in inflammation, nuclear factor kappa (NF-кB) and mitogen-activated protein kinases (MAPKs) are important. NF-kB is a diploid composed of p65 and IkBα and stimulates the pro- gene. MAPKs is a family consisting of the extracellular signal-regulated kinase (ERK), c-Jun NH2-terminal kinase (JNK), and p38, JNK and p38 play a role as proinflammatory mediators. Thus, we aim to determine the scutellarein (SCU) effect on LPS stimulated RAW264.7 cells. Furthermore, since scutellarein has been shown to inhibit the SARS coronavirus helicase and has been used in Chinese medicine to treat inflammatory disorders like COVID-19, it would be required to examine scutellarein’s anti-inflammatory mechanism. We identified inflammation-inducing substances using western blot with RAW264.7 cells and SCU. And we discovered that was reduced by treatment with SCU in p-p65 and p-IκBα. Also, we found that p-JNK and p-ERK were also decreased but there was no effect in p-p38. In addition, we have confirmed that the iNOS was also decreased after treatment but there is no change in the expression of COX-2. Therefore, this study shows that SCU can be used as a compound to treat inflammation.
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Affiliation(s)
- Min Yeong Park
- Research Institute of Life Science, College of Veterinary Medicine, Gyeongsang National University, Jinju 52828, Korea; (M.Y.P.); (S.E.H.); (H.H.K.); (P.B.B.); (A.A.); (S.H.J.)
| | - Sang Eun Ha
- Research Institute of Life Science, College of Veterinary Medicine, Gyeongsang National University, Jinju 52828, Korea; (M.Y.P.); (S.E.H.); (H.H.K.); (P.B.B.); (A.A.); (S.H.J.)
- Biological Resources Research Group, Gyeongnam Department of Environment Toxicology, Chemistry, Korea Institute of Toxicology, 17 Jegok-gil, Jinju 52834, Korea;
| | - Hun Hwan Kim
- Research Institute of Life Science, College of Veterinary Medicine, Gyeongsang National University, Jinju 52828, Korea; (M.Y.P.); (S.E.H.); (H.H.K.); (P.B.B.); (A.A.); (S.H.J.)
| | - Pritam Bhagwan Bhosale
- Research Institute of Life Science, College of Veterinary Medicine, Gyeongsang National University, Jinju 52828, Korea; (M.Y.P.); (S.E.H.); (H.H.K.); (P.B.B.); (A.A.); (S.H.J.)
| | - Abuyaseer Abusaliya
- Research Institute of Life Science, College of Veterinary Medicine, Gyeongsang National University, Jinju 52828, Korea; (M.Y.P.); (S.E.H.); (H.H.K.); (P.B.B.); (A.A.); (S.H.J.)
| | - Se Hyo Jeong
- Research Institute of Life Science, College of Veterinary Medicine, Gyeongsang National University, Jinju 52828, Korea; (M.Y.P.); (S.E.H.); (H.H.K.); (P.B.B.); (A.A.); (S.H.J.)
| | - Joon-Suk Park
- Preclinical Research Center, Daegu-Gyeonbuk Medical Innovation Foundation (DGMIF), 80 Cheombok-ro, Dong-gu, Daegu 41061, Korea;
| | - Jeong Doo Heo
- Biological Resources Research Group, Gyeongnam Department of Environment Toxicology, Chemistry, Korea Institute of Toxicology, 17 Jegok-gil, Jinju 52834, Korea;
| | - Gon Sup Kim
- Research Institute of Life Science, College of Veterinary Medicine, Gyeongsang National University, Jinju 52828, Korea; (M.Y.P.); (S.E.H.); (H.H.K.); (P.B.B.); (A.A.); (S.H.J.)
- Correspondence: ; Tel.: +82-55-772-2346
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Tan X, Gao L, Cai X, Zhang M, Huang D, Dang Q, Bao L. Vitamin D 3 alleviates cognitive impairment through regulating inflammatory stress in db/db mice. Food Sci Nutr 2021; 9:4803-4814. [PMID: 34531993 PMCID: PMC8441317 DOI: 10.1002/fsn3.2397] [Citation(s) in RCA: 1] [Impact Index Per Article: 0.3] [Reference Citation Analysis] [Abstract] [Key Words] [Grants] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 01/30/2021] [Revised: 05/18/2021] [Accepted: 05/26/2021] [Indexed: 12/12/2022] Open
Abstract
Patients with type 2 diabetes mellitus (T2DM) have a higher risk to develop cognitive impairment. Several studies reported the potential roles of vitamin D in prevention of cognitive impairment, but the mechanism remains unclear. The present study aims to investigate the protective effects of vitamin D3 on cognitive impairment in db/db mice and to explore the possible mechanism. Twelve-week-old male db/db mice were randomly administrated with low, medium, and high dose of vitamin D3 (LVD, MVD, and HVD groups, respectively) and equivalent volume vitamin D3 solvent (corn oil, DM group) intragastrically. Eight age-matched db/m mice were given equivalent volume corn oil as normal group. After 16 weeks of vitamin D3 treatment, the concentrations of fasting serum glucose in three vitamin D3 groups (especially the 1,000 IU/kg·bw dose) were significantly decreased compared with DM group. Pathology revealed that the neuron damage was reduced in vitamin D3 groups. MVD intervention significantly shortened the escape latency on day 5 and extended time in the target quadrant. Mice in HVD group had significantly higher exploration time and discrimination index compared with the DM group mice. Moreover, vitamin D3 treatment has increased the phosphorylation of cAMP-response element-binding protein and the expression of brain-derived neurotrophic factor and vitamin D receptor. This treatment, meanwhile, has decreased the expression of tumor necrosis factor-α, the phosphorylation of inhibitor kappa Bα (IκBα), and nuclear factor-κB p65 (NF-κB p65) in the hippocampus of db/db mice. These results suggest that vitamin D3 alleviated cognitive impairment in the hippocampus of db/db mice. Down-regulation of the NF-κB signaling pathway-related proteins IκBα and p65 might be one of the possible mechanisms.
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Affiliation(s)
- Xiaomu Tan
- Neurology DepartmentLuhe HospitalCapital Medical UniversityBeijingChina
| | - Lifang Gao
- School of Public HealthBeijing Key Laboratory of Environmental ToxicologyCapital Medical UniversityBeijingChina
| | - Xiaxia Cai
- School of Public HealthBeijing Key Laboratory of Environmental ToxicologyCapital Medical UniversityBeijingChina
| | - Mingyuan Zhang
- School of Public HealthBeijing Key Laboratory of Environmental ToxicologyCapital Medical UniversityBeijingChina
| | - Dongxu Huang
- School of Public HealthBeijing Key Laboratory of Environmental ToxicologyCapital Medical UniversityBeijingChina
| | - Qinyu Dang
- School of Public HealthBeijing Key Laboratory of Environmental ToxicologyCapital Medical UniversityBeijingChina
| | - Lei Bao
- Department of Clinical NutritionPeking University International HospitalBeijingChina
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Kamarya Y, Lijie X, Jinyao L. Chemical Constituents and their Anti-Tumor Mechanism of Plants from Artemisia. Anticancer Agents Med Chem 2021; 22:1838-1844. [PMID: 34238198 DOI: 10.2174/1871520621666210708125230] [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: 01/28/2021] [Revised: 05/16/2021] [Accepted: 05/23/2021] [Indexed: 11/22/2022]
Abstract
BACKGROUND At present, chemotherapy is still the main treatment method for cancer, but its side effects and multidrug resistance limit the therapeutic effect seriously. Now the screening of anti-tumor drugs with higher efficiency and lower toxicity from natural products is one of the important research directions for oncotherapy. Artemisia has a variety of anti-tumor constituents, which can exert its anti-tumor effect by inducing tumor cell apoptosis, inhibiting tumor angiogenesis, arresting cell cycle, accelerating iron ion-mediated oxidative damage, etc. Objective: This paper will provide a focused, up-to-date and comprehensive overview of the anti-tumor active constituents and their mechanisms of plants in Artemisia. METHOD The relevant information about Artemisia and its bioactive components comes from scientific databases (such as PubMed, Web of Science, Science Direct). RESULTS Here we have discussed the present situation and mechanism of bioactive components of Artemisia in anti-tumor. The application prospect of active components of Artemisia in cancer prevention and treatment was investigated. CONCLUSION The information summarized in this review may provide new ideas for the follow-up treatment of cancer and contribute to the development of new, effective, multi-side effects and fewer side effects of antineoplastic drugs.
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Affiliation(s)
- Yasin Kamarya
- Xinjiang Key Laboratory of Biological Resources and Genetic Engineering, College of Life Science and Technology, Xinjiang University, Urumqi, China
| | - Xia Lijie
- Xinjiang Key Laboratory of Biological Resources and Genetic Engineering, College of Life Science and Technology, Xinjiang University, Urumqi, China
| | - Li Jinyao
- Xinjiang Key Laboratory of Biological Resources and Genetic Engineering, College of Life Science and Technology, Xinjiang University, Urumqi, China
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Ali A, Lim J, Kim EH, Lee JH, Seong S, Kim W. Anti-Inflammatory Effects of Heat-Processed Artemisia capillaris Thunberg by Regulating I κB α/NF- κB Complex and 15-PGDH in Mouse Macrophage Cells. EVIDENCE-BASED COMPLEMENTARY AND ALTERNATIVE MEDICINE : ECAM 2021; 2021:5320314. [PMID: 34194517 PMCID: PMC8203361 DOI: 10.1155/2021/5320314] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Track Full Text] [Download PDF] [Figures] [Subscribe] [Scholar Register] [Received: 08/05/2020] [Accepted: 05/26/2021] [Indexed: 11/18/2022]
Abstract
Growing evidence suggests that dietary nutrients in herbs and plants are beneficial in improving inflammatory disorders. Artemisia capillaris Thunberg (AC) is a traditional herbal medicine widely used in East Asia to treat pain, hepatotoxicity, and inflammatory disorders. Heat processing is a unique pharmaceutical method used in traditional herbal medicine to enhance the pharmacological effects and safety of medicinal plants. This study demonstrates the anti-inflammatory effects of heat-processed AC (HPAC) in lipopolysaccharide- (LPS-) treated mouse macrophage cells. HPAC reduced LPS-induced inflammatory mediators such as IL-6, IL-1β, TNF-α, NO, and PGE2 in RAW 264.7 cells. Interestingly, 15-PGDH appears to play a pivotal role rather than COX-2 and mPGES-1 when HPAC regulated PGE2 levels. Meanwhile, HPAC showed anti-inflammatory effects by blocking IκBα phosphorylation and NF-κB nuclear translocalization. Also, we found that HO-1 upregulation was mediated by the mitogen-activated protein kinase (MAPK) pathways in HPAC-treated RAW 264.7 cells. And, in RAW 264.7 cells challenged with LPS, HPAC restored HO-1 expression, leading to NF-κB inhibition. Through further experiments using specific MAPK inhibitors, we found that, in response to LPS, the phosphorylated IκBα and activated NF-κB were attenuated by p38 MAPK/HO-1 pathway. Therefore, HPAC targeting both the IκBα/NF-κB complex and 15-PGDH may be considered as a potential novel anti-inflammatory agent derived from a natural source.
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Affiliation(s)
- Akhtar Ali
- Cnh Center for Cancer Research, Gangnam-gu, Seoul 06154, Republic of Korea
| | - Junsik Lim
- Division of Pharmacology, College of Korean Medicine, Semyung University, Jecheon 27136, Republic of Korea
| | - En Hyung Kim
- Department of Dermatology, Bundang Jesaeng General Hospital, Seongnam, Gyeonggi 13590, Republic of Korea
| | - Jong-Hyun Lee
- Department of Natural Medicine, College of Pharmacy, Dongduk Women's University, Seongbuk-gu, Seoul 02748, Republic of Korea
| | - Shin Seong
- Soram Korean Medicine Hospital, Gangnam-gu, Seoul 06154, Republic of Korea
| | - Wonnam Kim
- Cnh Center for Cancer Research, Gangnam-gu, Seoul 06154, Republic of Korea
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Jia H, Liu Y, Guo D, He W, Zhao L, Xia S. PM2.5-induced pulmonary inflammation via activating of the NLRP3/caspase-1 signaling pathway. ENVIRONMENTAL TOXICOLOGY 2021; 36:298-307. [PMID: 32996690 PMCID: PMC7891361 DOI: 10.1002/tox.23035] [Citation(s) in RCA: 92] [Impact Index Per Article: 23.0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Subscribe] [Scholar Register] [Received: 04/23/2020] [Revised: 09/15/2020] [Accepted: 09/15/2020] [Indexed: 05/07/2023]
Abstract
Particulate matter 2.5 (PM2.5)-induced pulmonary inflammation has become a public concern in recent years. In which, the activation of the NLRP3/caspase-1 pathway was closely related to the inflammatory response of various diseases. However, the promotion effect of the NLRP3/caspase-1 pathway on PM2.5-induced pulmonary inflammation remains largely unclear. Here, our data showed that PM2.5 exposure caused lung injury in the mice by which inflammatory cell infiltration occurred in lung and alveolar structure disorder. Meanwhile, the exposure of human bronchial epithelial cells (16HBE) to PM2.5 resulted in suppressed cell viability, as well as elevated cell apoptosis. Moreover, a higher level of inflammatory cytokine and activation of the NLRP3/caspase-1 pathway in PM2.5-induced inflammation mice models and 16HBE cells. Mechanistically, pretreatment with MCC950, a NLRP3/caspase-1 pathway inhibitor, prevented PM2.5-induced lung injury, inflammatory response, and the number of inflammatory cells in BALFs, as well as promoted cell viability and decreased inflammatory cytokine secretion. Collectively, our findings indicated that the NLRP3/caspase-1 pathway serves a vital role in the pathological changes of pulmonary inflammation caused by PM2.5 exposure. MCC950 was expected to be the therapeutic target of PM2.5 inhalation mediated inflammatory diseases.
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Affiliation(s)
- Hui Jia
- Department of Respiratory and Critical Care MedicineCentral Hospital Affiliated to Shenyang Medical CollegeShenyangChina
| | - Yang Liu
- Department of Respiratory and Critical Care MedicineCentral Hospital Affiliated to Shenyang Medical CollegeShenyangChina
| | - Dan Guo
- Department of Respiratory and Critical Care MedicineCentral Hospital Affiliated to Shenyang Medical CollegeShenyangChina
| | - Wei He
- Department of Respiratory and Critical Care MedicineCentral Hospital Affiliated to Shenyang Medical CollegeShenyangChina
| | - Long Zhao
- Department of Respiratory and Critical Care MedicineCentral Hospital Affiliated to Shenyang Medical CollegeShenyangChina
| | - Shuyue Xia
- Department of Respiratory and Critical Care MedicineCentral Hospital Affiliated to Shenyang Medical CollegeShenyangChina
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Kostoff RN, Briggs MB, Shores DR. Treatment repurposing for inflammatory bowel disease using literature-related discovery and innovation. World J Gastroenterol 2020; 26:4889-4899. [PMID: 32952337 PMCID: PMC7476176 DOI: 10.3748/wjg.v26.i33.4889] [Citation(s) in RCA: 7] [Impact Index Per Article: 1.4] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Download PDF] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 05/05/2020] [Revised: 05/21/2020] [Accepted: 08/27/2020] [Indexed: 02/06/2023] Open
Abstract
Inflammatory bowel disease (IBD) incidence has been increasing steadily, most dramatically in the Western developed countries. Treatment often includes lifelong immunosuppressive therapy and surgery. There is a critical need to reduce the burden of IBD and to discover medical therapies with better efficacy and fewer potential side-effects. Repurposing of treatments originally studied in other diseases with similar pathogenesis is less costly and time intensive than de novo drug discovery. This study used a treatment repurposing methodology, the literature-related discovery and innovation (LRDI) text mining system, to identify potential treatments (developed for non-IBD diseases) with sufficient promise for extrapolation to treatment of IBD. By searching for desirable patterns of twenty key biomarkers relevant to IBD (e.g., inflammation, reactive oxygen species, autophagy, barrier function), the LRDI-based query retrieved approximately 9500 records from Medline. The most recent 350 records were further analyzed for proof-of-concept. Approximately 18% (64/350) met the criteria for discovery (not previously studied in IBD human or animal models) and relevance for application to IBD treatment. Many of the treatments were compounds derived from herbal remedies, and the majority of treatments were being studied in cancer, diabetes, and central nervous system disease, such as depression and dementia. As further validation of the search strategy, the query identified ten treatments that have just recently begun testing in IBD models in the last three years. Literature-related discovery and innovation text mining contains a unique search strategy with tremendous potential to identify treatments for repurposing. A more comprehensive query with additional key biomarkers would have retrieved many thousands more records, further increasing the yield of IBD treatment repurposing discovery.
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Affiliation(s)
- Ronald Neil Kostoff
- School of Public Policy, Georgia Institute of Technology, Gainesville, VA 20155, United States
| | | | - Darla Roye Shores
- The Hopkins Resource for Intestinal Vitality and Enhancement, the Johns Hopkins University School of Medicine, Baltimore, MD 21287, United States
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