• Cancer
• Metabolic disorder
• PES1
• TME

• Humans
• Animals
• Neoplasms/metabolism
• Neoplasms/drug therapy
• Neoplasms/genetics
• RNA-Binding Proteins/metabolism
• RNA-Binding Proteins/genetics
• Diabetes Mellitus, Type 2/metabolism
• Diabetes Mellitus, Type 2/genetics
• Diabetes Mellitus, Type 2/drug therapy
• Tumor Microenvironment
• Lipid Metabolism
• Molecular Targeted Therapy/methods
• Obesity/metabolism
• Obesity/genetics

• Autophagy
• Clinically relevant implementation
• Human disease
• Molecular mechanism
• Selective autophagy
• Small-molecule drug

• Humans
• Autophagy/drug effects
• Animals
• Neurodegenerative Diseases/drug therapy
• Neurodegenerative Diseases/metabolism
• Neoplasms/drug therapy
• Neoplasms/metabolism
• Metabolic Diseases/drug therapy
• Metabolic Diseases/metabolism
• Cardiovascular Diseases/drug therapy
• Cardiovascular Diseases/metabolism

• Diosgenin
• Liver regeneration
• Network pharmacology
• Rhizoma Dioscoreae

• Xiaoyao san (XYS)
• in vivo experiments
• metabolomics
• network pharmacology
• nonalcoholic fatty liver disease (NAFLD)
• systems biology

• Animals
• Non-alcoholic Fatty Liver Disease/drug therapy
• Non-alcoholic Fatty Liver Disease/metabolism
• Drugs, Chinese Herbal/pharmacology
• Molecular Docking Simulation
• Rats
• Metabolomics
• Liver/metabolism
• Liver/drug effects
• Liver/pathology
• Computational Biology/methods
• Spleen/metabolism
• Spleen/drug effects
• Spleen/pathology
• Disease Models, Animal
• Male
• PPAR gamma/metabolism
• Cyclooxygenase 2/metabolism

• Farnesoid X Receptor
• Natural Products
• Nonalcoholic Fatty Liver Disease
• Review

• Humans
• Non-alcoholic Fatty Liver Disease/drug therapy
• Non-alcoholic Fatty Liver Disease/genetics
• Non-alcoholic Fatty Liver Disease/metabolism
• Receptors, Cytoplasmic and Nuclear/genetics
• Receptors, Cytoplasmic and Nuclear/metabolism
• Receptors, Cytoplasmic and Nuclear/pharmacology
• Liver/metabolism

• Non-alcoholic fatty liver disease
• Pathogenesis
• Traditional Chinese medicine
• Treatment strategies
• Western medicine

• 82070590 National Natural Science Foundation of China
• 82373930 National Natural Science Foundation of China

• Autophagy
• Hepatic stellate cells
• Hepatocytes
• Macrophages
• Non-alcoholic fatty liver disease

• IA/I/16/2/502691 DBT-Wellcome Trust India Alliance

• autophagy
• bioactive compounds
• inflammation
• lipid metabolism

• Humans
• Non-alcoholic Fatty Liver Disease/drug therapy
• Non-alcoholic Fatty Liver Disease/metabolism
• Lipid Metabolism
• Oxidative Stress
• Polyphenols/metabolism
• Autophagy
• Liver/metabolism

• Functional food
• NASH
• Seaweeds

• National Natural Science Foundation of China
• Sichuan Science and Technology Innovation Seedling Project
• Basic and Applied Basic Research Foundation of Guangdong Province
• Fundamental Research Funds for the Central Universities
• China Postdoctoral Science Foundation

• Resveratrol
• anti-aging
• chronic diseases
• inflammation
• molecular targets

• AMPK
• Coix lacryma-jobi L.
• intestinal flora
• lipid homeostasis
• non-alcoholic fatty liver disease
• polyphenol

• Mice
• Animals
• Coix/metabolism
• Polyphenols/pharmacology
• Polyphenols/metabolism
• Gastrointestinal Microbiome
• Non-alcoholic Fatty Liver Disease/etiology
• AMP-Activated Protein Kinases/metabolism
• Glucose/metabolism
• Liver/metabolism
• Lipid Metabolism
• Triglycerides/metabolism
• Hypercholesterolemia/metabolism
• Homeostasis

Metformin (MET) has been proved to be effective for the treatment of psoriasis. The mechanisms of its action under the hyperlipidemia have yet to be fully elucidated. Here, we investigated the effect of metformin on the cell proliferation induced by hyperlipidemia and the underlying mechanism in immortalized human keratinocyte cell line (HaCat).

Wild-type or FOXO3 knockdown HaCat cells were treated with free fatty acids (FFA) for 10 days and then co-treated with metformin for another 4 days. Triglyceride (TG) level, cell viability, proliferation, apoptosis, antioxidant enzymes, reactive oxygen species (ROS) levels, as well as the transcription activity of FOXO3 were analyzed.

Metformin decreased HaCaT cell proliferation and induced cell apoptosis after FFA treatment. Metformin was found to significantly increase the expressions and the activities of superoxide dismutase (SOD) as well as catalase (CAT), and reduced the reactive oxygen species (ROS) level. Metformin significantly promoted the autophagy and increase FOXO3 protein level in the nucleus under hyperlipidemia. However, all of the effects from metformin were partially blocked by FOXO3 knockdown.

This study demonstrated that under the hyperlipidemia, metformin has significant antiproliferation and proapoptosis effects by reducing ROS level as well as increasing autophagy. All of these effects from metformin were through FOXO3-dependent pathway.

• FOXO3
• ROS
• apoptosis
• autophagy
• forkhead box O3
• reactive oxygen species

The breadth and depth of traditional Chinese medicine (TCM) applications have been expanding in recent years, yet the problem of quality control has arisen in the application process. It is essential to design an algorithm to provide blending ratios that ensure a high overall product similarity to the target with controlled deviations in individual ingredient content. We developed a new blending algorithm and scheme by comparing different samples of ginkgo leaves. High-consistency samples were used to establish the blending target, and qualified samples were used for blending. Principal component analysis (PCA) was used as the sample screening method. A nonlinear programming algorithm was applied to calculate the blending ratio under different blending constraints. In one set of calculation experiments, the result was blended by the same samples under different conditions. Its relative deviation coefficients (RDCs) were controlled within ±10%. In another set of calculations, the RDCs of more component blending by different samples were controlled within ±20%. Finally, the near-critical calculation ratio was used for the actual experiments. The experimental results met the initial setting requirements. The results show that our algorithm can flexibly control the content of TCMs. The quality control of the production process of TCMs was achieved by improving the content stability of raw materials using blending. The algorithm provides a groundbreaking idea for quality control of TCMs.

• Chromatography, High Pressure Liquid
• Drugs, Chinese Herbal/analysis
• Ginkgo biloba
• Medicine, Chinese Traditional
• Plant Leaves/chemistry
• Quality Control

• autophagy
• lipophagy
• mitophagy
• reticulophagy
• non-alcoholic fatty liver disease

There have been significant advances, particularly over the last 20 years, in the identification of non-coding RNAs (ncRNAs) and their pathophysiological role in a wide range of disease states, particularly cancer and other chronic conditions characterized by excess inflammation and oxidative stress such as atherosclerosis, diabetes, obesity, multiple sclerosis, osteoporosis, liver and lung fibrosis. Such discoveries have potential therapeutic implications as a better understanding of the molecular mechanisms underpinning the effects of ncRNAs on critical homeostatic control mechanisms and biochemical pathways might lead to the identification of novel druggable targets. In this context, increasing evidence suggests that several natural compounds can target ncRNAs at different levels and, consequently, influence processes involved in the onset and progression of disease states. The natural phenol resveratrol has been extensively studied for therapeutic purposes in view of its established anti-inflammatory and antioxidant effects, particularly in disease states such as cancer and cardiovascular disease that are associated with human aging. However, increasing in vitro and in vivo evidence also suggests that resveratrol can directly target various ncRNAs and that this mediates, at least in part, its potential therapeutic effects. This review critically appraises the available evidence regarding the resveratrol-mediated modulation of different ncRNAs in a wide range of disease states characterized by a pro-inflammatory state and oxidative stress, the potential therapeutic applications, and future research directions.

• Università degli Studi di Sassari
• University of Sharjah

• Cornus officinalis vinegar
• anti-oxidant activity
• hepatic steatosis
• liver function
• nonalcoholic fatty liver disease

Liver fibrosis is a disease with complex pathological mechanisms. Penthorum chinense Pursh (P. chinense) is a traditional Chinese medicine (TCM) for liver injury treatment. However, the pharmacological mechanisms of P. chinense on liver fibrosis have not been investigated and clarified clearly. This study was designed to investigate the chemicals in P. chinense and explore its effect on liver fibrosis. First, we developed a highly efficient method, called DDA-assisted DIA, which can both broaden mass spectrometry (MS) coverage and MS² quality. In DDA-assisted DIA, data-dependent acquisition (DDA) and data-independent acquisition (DIA) were merged to construct a molecular network, in which 1,094 mass features were retained in Penthorum chinense Pursh (P. chinense). Out of these, 169 compounds were identified based on both MS¹ and MS² analysis. After that, based on a network pharmacology study, 94 bioactive compounds and 440 targets of P. chinense associated with liver fibrosis were obtained, forming a tight compound–target network. Meanwhile, the network pharmacology experimental results showed that multiple pathways interacted with the HIF-1 pathway, which was first identified involved in P. chinense. It could be observed that some proteins, such as TNF-α, Timp1, and HO-1, were involved in the HIF-1 pathway. Furthermore, the pharmacological effects of P. chinense on these proteins were verified by CCl₄-induced rat liver fibrosis, and P. chinense was found to improve liver functions through regulating TNF-α, Timp1, and HO-1 expressions. In summary, DDA-assisted DIA could provide more detailed compound information, which will help us to annotate the ingredients of TCM, and combination with computerized network pharmacology provided a theoretical basis for revealing the mechanism of P. chinense.

• DDA-assisted DIA
• Penthorum chinense
• action of mechanism
• liver fibrosis
• network pharmacology

• Meta-analysis
• Non-alcoholic fatty liver disease
• Systematic review
• Traditional Chinese medicine
• Xiaoyao Powder

• Biomarkers/blood
• Drugs, Chinese Herbal/adverse effects
• Drugs, Chinese Herbal/pharmacology
• Humans
• Non-alcoholic Fatty Liver Disease/drug therapy
• Randomized Controlled Trials as Topic

Non-alcoholic fatty liver disease (NAFLD) is among the most prevalent primary liver diseases worldwide and can develop into various conditions, ranging from simple steatosis, through non-alcoholic steatohepatitis (NASH), to fibrosis, and eventually cirrhosis and hepatocellular carcinoma. Nevertheless, there is no effective treatment for NAFLD due to the complicated etiology. Recently, activation of the NLPR3 inflammasome has been demonstrated to be a contributing factor in the development of NAFLD, particularly as a modulator of progression from initial hepatic steatosis to NASH. NLRP3 inflammasome, as a caspase-1 activation platform, is critical for processing key pro-inflammatory cytokines and pyroptosis. Various stimuli involved in NAFLD can activate the NLRP3 inflammasome, depending on the diverse cellular stresses that they cause. NLRP3 inflammasome-related inhibitors and agents for NAFLD treatment have been tested and demonstrated positive effects in experimental models. Meanwhile, some drugs have been applied in clinical studies, supporting this therapeutic approach. In this review, we discuss the activation, biological functions, and treatment targeting the NLRP3 inflammasome in the context of NAFLD progression. Specifically, we focus on the different types of therapeutic agents that can inhibit the NLRP3 inflammasome and summarize their pharmacological effectiveness for NAFLD treatment.

• NAFLD
• NASH
• NLRP3
• inflammasome
• therapeutic agents

Lycium barbarum berries have been utilized in Asia for many years. However, the mechanisms of its lung-defensive properties are indeterminate.

We investigate whether L. barbarum polysaccharide (LBP) could weaken Pseudomonas aeruginosa infection-induced lung injury.

Mice primary air-liquid interface epithelial cultures were pretreated with LBP and subsequently treated with pyocyanin (PCN). Lung injury, including apoptosis, inflammation, and oxidative stress, was estimated by western blot, enzyme-linked immunosorbent assay, and real-time quantitative polymerase chain reaction, Real-time qPCR (Q-PCR). Flow cytometry was used to test cell apoptosis. Moreover, Balb/c mice were used to evaluate the tissue injury. We used hematoxylin-eosin staining and immunofluorescence to detect the expression of related proteins and tissue damage in mouse lungs and spleen.

The flow cytometric analysis shows the potential of LBP to reduce time-dependent cell death by PCN. Mechanistically, LBP reduces PCN-induced expression of proapoptotic proteins and caspase3 and induces the activation of Bcl-2 in mice bronchial epithelial cells. Similarly, LBP reduces PCN-induced intracellular reactive oxygen species (ROS) production. Moreover, LBP inhibits the production of inflammatory cytokines, Interleukin (IL-1β), Tumor Necrosis Factor (TNF), IL-6, and IL-8. Our study confirms the ability of LBP to retard PCN-induced injury in mice lung and spleen.

The inhibition of PCN-induced lung injury by LBP is capable of protecting mice cells from injury.

Lipids work as essential energy sources for organisms. However, prawns fed on high-fat diets suffer from oxidative stress, whose potential mechanisms are poorly understood. The present study aimed to explore the regulation mechanism of oxidative stress induced by high fat and the amelioration by vitamin E (VE) of oxidative stress. Macrobrachium rosenbergii were fed with two dietary fat levels (LF 9% and HF 13%) and two VE levels (200 mg/kg and 600 mg/kg) for 8 weeks. The results showed that the HF diet decreased the growth performance, survival rate and antioxidant capacity of M. rosenbergii, as well as inducing hypertrophied lipid droplets, lipophagy and apoptosis. A total of 600 mg/kg of VE in the HF diet alleviated the negative effects induced by HF. In addition, the HF diet suppressed the expression of toll-dorsal and imd-relish signal pathways. After the relish and dorsal pathways were knocked down, the downstream iNOS and NO levels decreased and the MDA level increased. The results indicated that M. rosenbergii fed with a high-fat diet could cause oxidative damage. Its molecular mechanism may be attributed to the fact that high fat suppresses the NF-κB/NO signaling pathway mediating pro-oxidant and antioxidant targets for regulation of oxidative stress. Dietary VE in an HF diet alleviated hepatopancreas oxidative stress and apoptosis.

• Macrobrachium rosenbergii
• NF-κB
• high fat diet
• oxidative stress
• vitamin E

• Apoptosis
• cancer
• dioscin
• fungal
• liver injury
• metabolism
• pharmacological
• saponin
• viral

• Diosgenin/analogs & derivatives
• Diosgenin/chemistry
• Diosgenin/pharmacology
• Diosgenin/therapeutic use
• Humans
• Neoplasms/drug therapy
• Plant Extracts/chemistry
• Saponins

• Cardiac hypertrophy
• Dioscin
• ERK
• Isoproterenol
• Oxidative stress
• PKCε signal

• Animals
• Diosgenin/analogs & derivatives
• Diosgenin/pharmacology
• Diosgenin/therapeutic use
• Isoproterenol/toxicity
• Oxidative Stress/drug effects
• Cardiomegaly/chemically induced
• Cardiomegaly/drug therapy
• Cardiomegaly/prevention & control
• Cardiomegaly/metabolism
• Cardiomegaly/pathology
• Rats
• Protein Kinase C-epsilon/metabolism
• Male
• Myocytes, Cardiac/drug effects
• Myocytes, Cardiac/metabolism
• Myocytes, Cardiac/pathology
• Cell Line
• MAP Kinase Signaling System/drug effects
• Rats, Sprague-Dawley
• Cardiotonic Agents/pharmacology
• Cardiotonic Agents/therapeutic use
• Extracellular Signal-Regulated MAP Kinases/metabolism

The present study aimed to investigate the protective effect of carvacrol on liver injury in mice with type 2 diabetes mellitus (T2DM) and to assess its potential molecular mechanism. Mice were divided into three groups (n=15/group): Non-diabetic db/m+ mice group, db/db mice group and db/db mice + carvacrol group. In the db/db mice + carvacrol group, db/db mice were administered 10 mg/kg carvacrol daily by gavage for 6 weeks. Fasting blood glucose and insulin levels were separately examined. Pathological changes were observed using hematoxylin and eosin, Masson's trichrome, periodic acid Schiff and reticular fiber staining. In addition, immunohistochemistry, immunofluorescence and western blotting were used to examine the expression levels of Toll-like receptor 4 (TLR4), NF-κB, NALP3, AKT1, phosphorylated (p)-AKT1, insulin receptor (INSR), p-INSR, mTOR, p-mTOR, insulin receptor substrate 1 (IRS1) and p-IRS1 in the liver tissues. The results revealed that carvacrol improved blood glucose and insulin resistance of T2DM db/db mice. After treatment with carvacrol for 6 weeks, the serum levels of TC, TG and LDL-C were markedly reduced, whereas HDL-C levels were significantly increased in db/db mice. Furthermore, carvacrol administration significantly decreased serum ALT and AST levels in db/db mice. Serum BUN, Cre and UA levels were markedly higher in db/db mice compared with those in the control group; however, carvacrol treatment markedly reduced their serum levels in db/db mice. Furthermore, histological examinations confirmed that carvacrol could protect the liver of db/db mice. Carvacrol could ameliorate liver injury induced by T2DM via mediating insulin, TLR4/NF-κB and AKT1/mTOR signaling pathways. The present findings suggested that carvacrol exerted protective effects on the liver in T2DM db/db mice, which could be related to insulin, TLR4/NF-κB and AKT1/mTOR signaling pathways.

• T2DM
• blood glucose
• carvacrol
• insulin resistance
• liver injury

• Krüppel‑like Factor 4
• asthma
• inflammation
• isoalantolactone
• macrophage
• peroxisome proliferator‑activated receptor γ

• HIPPO pathway
• inflammation
• lipid metabolism
• liver fibrosis
• metabolic dysfunction‑associated fatty liver disease
• parthenolide

• Animals
• Disease Models, Animal
• Fibrosis/drug therapy
• Fibrosis/genetics
• Fibrosis/metabolism
• Hippo Signaling Pathway
• Inflammation/drug therapy
• Inflammation/genetics
• Inflammation/metabolism
• Lipid Metabolism/drug effects
• Lipid Metabolism/genetics
• Male
• Metabolic Diseases/complications
• Mice, Inbred C57BL
• Non-alcoholic Fatty Liver Disease/drug therapy
• Non-alcoholic Fatty Liver Disease/etiology
• Non-alcoholic Fatty Liver Disease/metabolism
• Non-alcoholic Fatty Liver Disease/pathology
• Oxidative Stress/drug effects
• Protective Agents/pharmacology
• Protective Agents/therapeutic use
• Protein Serine-Threonine Kinases/metabolism
• Sesquiterpenes/pharmacology
• Sesquiterpenes/therapeutic use
• Signal Transduction/drug effects
• Mice

• Buchholzia coriacea seed
• inflammation
• insulin resistance
• metabolic dysfunction
• mouse
• non-alcoholic fatty liver disease (NAFLD)
• oxidative stress
• phytotherapy
• steatosis

• Apoptosis
• Autophagy
• Ferroptosis
• Metabolic dysfunction-associated fatty liver disease
• Necroptosis
• Pyroptosis

• Apoptosis
• Autophagy
• Exercise Therapy
• Fatty Liver/metabolism
• Fatty Liver/pathology
• Fatty Liver/therapy
• Humans
• Lipid Metabolism
• MicroRNAs/metabolism
• Necroptosis
• Receptors, Death Domain/metabolism
• Signal Transduction

• 81830119 National Natural Science Foundation of China
• 81673750 National Natural Science Foundation of China

Background: Non-alcoholic fatty liver disease (NAFLD), characterized by the excessive accumulation of hepatic triglycerides (TGs), has become a worldwide chronic liver disease. But efficient therapy keeps unsettled. Our previous works show that geniposide and chlorogenic acid combination (namely the GC combination), two active chemical components combined with a unique ratio (67.16:1), presents beneficial effects on high-fat diet-induced NAFLD rodent models. Notably, microarray highlighted the more than 5-fold down-regulated SCD-1 gene in the GC combination group. SCD-1 is an essential lipogenic protein for monounsaturated fatty acids’ biosynthesis and serves as a key regulatory enzyme in the last stage of hepatic de novo lipogenesis (DNL).

Methods: NAFLD mice model was fed with 16 weeks high-fat diet (HFD). The pharmacological effects, primarily on hepatic TG, TC, FFA, and liver enzymes, et al. of the GC combination and two individual components were evaluated. Furthermore, hepatic SCD-1 expression was quantified with qRT-PCR, immunoblotting, and immunohistochemistry. Finally, the lentivirus-mediated over-expressed cell was carried out to confirm the GC combination’s influence on SCD-1.

Results: The GC combination could significantly reduce hepatic TG, TC, and FFA in NAFLD rodents. Notably, the GC combination presented synergetic therapeutic effects, compared with two components, on normalizing murine hepatic lipid deposition and disordered liver enzymes (ALT and AST). Meanwhile, the robust SCD-1 induction induced by HFD and FFA in rodents and ALM-12 cells was profoundly blunted, and this potent suppression was recapitulated in lentivirus-mediated SCD-1 over-expressed cells.

Conclusion: Taken together, our data prove that the GC combination shows a substantial and synergetic anti-lipogenesis effect in treating NAFLD, and these amelioration effects are highly associated with the potent suppressed hepatic SCD-1 and a blunted DNL process.

• chlorogenic acid
• de novo lipogenesis
• geniposide
• metabolic associated fatty liver disease 1
• non alcoholic fatty liver disease
• stearoyl-CoA desaturase-1

Many studies have shown that resveratrol has a lot of therapeutic effects on liver disorders. Its administration can significantly increase the survival rate after liver transplantation, reduce fat deposition and ischemia-induced necrosis and apoptosis in Wistar rats. Resveratrol can provide Liver protection against chemical, cholestatic, and alcohol-mediated damage. It can improve glucose metabolism and lipid profile, reduce liver fibrosis, and steatosis. Additionally, it is capable of altering the fatty acid composition of the liver cells. Resveratrol may be a potential treatment option for the management of non-alcoholic fatty liver disease (NAFLD) due to its anti-inflammatory, antioxidant, and calorie-restricting effects. There are also studies that have evaluated the effect of resveratrol on lipid and liver enzyme profiles among patients with metabolic syndrome (MetS) and related disorders. Based on the extent of liver disease worldwide and the need to find new treatment possibilities, this review critically examines current in vitro and in vivo preclinical studies and human clinical studies related to liver protection.

• non-alcoholic fatty liver disease
• nutraceutical
• oxidative stress
• resveratrol

• Dietary supplements
• NAFLD
• Natural products
• Non-alcoholic fatty liver disease

• Autophagy
• Neurodegenerative disease
• Neuroprotection
• Traditional Chinese medicine

• Capsaicin
• M1 macrophages
• Notch signaling
• TNF-α
• liver fibrosis

Liver fibrosis (LF) is a healing response to wounds resulting in liver injury that can cause liver failure or even cancer without functional prevention. Resveratrol (RSV) has been suggested to exert biological effects against various human diseases. MicroRNA-20a (miRNA/miR-20a) has been shown to promote disease progression. The present study aimed to assess the mechanisms through which RSV induces autophagy and activates the miR-20a-mediated phosphatase and tensin homolog (PTEN)/PI3K/AKT signaling pathway in LF. First, a rat model of carbon tetrachlo-ride (CCL₄)-induced LF and a cell model of platelet-derived growth factor (PDGF)-BB-stimulated HSC-T6 cells were established for use in subsequent experiments. Subsequently, RSV at a range of concentrations was injected into the model rats with LF. Indicators related to liver injury, oxidative stress and fibrosis were determined in the rats with LF. The RSV-treated HSC-T6 cells were subjected to transfection with miR-20a mimic and PTEN overexpression plasmid to assess the levels of liver injury and LF. A dual-luciferase reporter gene assay was performed to verify the binding sites between PTEN and miR-20a. RSV was found to alleviate LF in rats, and autophagy was enhanced in the rats with LF following RSV treatment. Furthermore, the activation of the PTEN/PI3K/AKT axis attenuated LF, which was reversed by transfection with miR-20a mimic. RSV reversed the inhibitory effects of miR-20a on PTEN expression, reducing miR-20a expression and promoting PTEN, PI3K and p-AKT protein expression, thus attenuating LF. On the whole, the present study demonstrates that RSV induces autophagy and activates the miR-20a-mediated PTEN/PI3K/AKT signaling pathway to attenuate LF. These findings may lead to the development of potential therapeutic strategies for LF.

• CPT1A
• Inflammation
• MCD
• NAFLD
• STR

• Alanine Transaminase/blood
• Alkaloids/analysis
• Animals
• Cell Line
• Diet/adverse effects
• Drugs, Chinese Herbal/chemistry
• Drugs, Chinese Herbal/pharmacology
• Fatty Acids, Nonesterified/metabolism
• Humans
• Liver Cirrhosis/drug therapy
• Liver Cirrhosis/genetics
• Liver Cirrhosis/metabolism
• Male
• Mice, Inbred C57BL
• Non-alcoholic Fatty Liver Disease/drug therapy
• Non-alcoholic Fatty Liver Disease/metabolism
• Plant Extracts/pharmacology
• Quinolizines/analysis
• Sophora/chemistry
• Triglycerides/blood
• Triglycerides/metabolism
• Water/chemistry
• Matrines

• autophagosomes
• betaine
• mitochondria
• nonalcoholic fatty liver disease
• ultrastructure

• Animals
• Betaine/pharmacology
• Choline/metabolism
• Collagen
• Diet
• Dietary Supplements
• Disease Models, Animal
• Hepatocytes/drug effects
• Hepatocytes/ultrastructure
• Liver/drug effects
• Liver/ultrastructure
• Male
• Methionine/deficiency
• Mice
• Mice, Inbred C57BL
• Non-alcoholic Fatty Liver Disease/pathology

Nonalcoholic fatty liver disease (NAFLD) is a common chronic liver disease worldwide, and its incidence is increasing annually, but there is currently no specific drug for treating NAFLD. Shenling Baizhu powder (SL) is a safe herbal compound commonly used in clinical practice. Our previous research has shown that SL has the effect of preventing NAFLD, but its specific mechanism has not been determined. In this study, the potential mechanism of SL on NAFLD was explored by in vivo experiments.

Wistar rats fed a choline-deficient amino acid-defined diet (CDAA) were treated with SL for 8 weeks. Then, serum samples were collected to obtain biochemical indicators; adipose tissue and liver samples were collected for pathological detection; a moorFLPI-2 blood flow imager was used to measure liver microcirculation blood flow, and a rat cytokine array was used to screen potential target proteins. The expression of liver adiponectin/SREBP-1c pathway-related proteins was determined by Western blotting.

SL effectively reduced the liver wet weight, as well as the levels of total cholesterol (TC) and triglyceride (TG) in the liver, and ameliorated liver injury in CDAA-fed rats. Pathological examinations showed that SL markedly reduced liver lipid droplets and improved liver lipid accumulation. In addition, the detection of liver blood flow showed that SL increased liver microcirculation in CDAA-fed rats. Through the cytokine array, a differentially expressed cytokine, namely, adiponectin, was screened in the liver. Western blotting assays showed that SL increased the expression of adiponectin and phosphoacetyl-CoA Carboxylase (p-ACC) in the liver and decreased the expression of steroid regulatory element-binding protein-1c (SREBP-1c) and fatty acid synthase (FAS).

These results suggest that SL can increase the levels of adiponectin in the liver and serum and can inhibit the expression of SREBP-1c, thereby regulating systemic lipid metabolism and reducing liver lipid accumulation.

• fucoidan
• hypolipidemic effect
• mannan
• polysaccharide
• β-glucan

• Gene Expression Regulation/drug effects
• Gene Regulatory Networks/drug effects
• Hexosaminidases/metabolism
• Humans
• Hyperlipidemias/diet therapy
• Hyperlipidemias/metabolism
• Hypolipidemic Agents/pharmacology
• Hypolipidemic Agents/therapeutic use
• Lectins, C-Type/metabolism
• Mannans/pharmacology
• Mannans/therapeutic use
• Polysaccharides/pharmacology
• Polysaccharides/therapeutic use
• Toll-Like Receptors/metabolism
• beta-Glucans/pharmacology
• beta-Glucans/therapeutic use

• autophagy
• lipid droplet
• lipid homeostasis
• lipophagy
• non-alcoholic fatty liver disease

• Animals
• Autophagy
• Homeostasis
• Humans
• Lipogenesis
• Non-alcoholic Fatty Liver Disease/pathology
• Non-alcoholic Fatty Liver Disease/therapy

• Lycium barbarum polysaccharides
• antioxidant
• nuclear factor (erythroid-derived 2)-like 2 (Nrf2)
• osteoarthritis