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ORIGINAL ARTICLE
Year : 2017  |  Volume : 13  |  Issue : 50  |  Page : 245-253

Prevention mechanism of 2,3,5,4'-tetrahydroxy-stilbene-2-O-β-D-glucoside on lipid accumulation in steatosis hepatic L-02 cell


1 Department of Pharmacy, Yunnan University of Traditional Chinese Medicine, Kunming, Yunnan, China; Department of Oriental Medicinal Material and Processing, College of Life Science, Kyung Hee University, Yongin, South Korea
2 Department of Pharmacy, Yunnan University of Traditional Chinese Medicine, Kunming, Yunnan, China

Correspondence Address:
Dr. Jie Yu
Department of Pharmacy, Yunnan University of Traditional Chinese Medicine, Kunming, Yunnan
China
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/0973-1296.204563

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Aim: 2,3,5,4'-Tetrahydroxy-stilbene-2-O-β-d-glucoside (TSG), a natural stilbene, shows great activities in hepatic lipid regulation, especially for hepatic triglyceride lowering. However, information about its mechanisms on biosynthesis and degradation of triglyceride is still limited. This research pays close attention to clarify the mechanism of TSG on prevention of hepatic lipid accumulation. Materials and Methods: TSG was given to steatosis hepatocyte L-02 cell induced by fat emulsion incubation. The contents of free fatty acid, triglyceride, rate-controlling enzymes, and transcriptional regulatory factors, which play key role in biosynthesis and decomposition of triglyceride, were determined with or without TSG exposure. Results: TSG could reduce the free fatty acid material supply for the synthesis of endogenous triglyceride and it did so by reducing the expression of liver type fatty acid binding protein and fatty acid transport protein 4. TS Ginhibited the expression of sterol regulatory element-binding protein 1c, and then reduce the contents of acetyl-CoA carboxylase 1 and fatty acid synthase. Therefore,TSG prevented biosynthesis of triglyceride. Mean while, TSG also promoted the decomposition of triglyceride by the activation of peroxisome proliferators activator receptors alpha. Conclusion: TSG could effective intervene the accumulation of triglyceride in hepatic cell. Thus, TSG could be considered as a promising drug candidate in prevention and treatment of lipid metabolic disorders, especially nonalcoholic fatty liver disease. Abbreviations used: ACACA: Acetyl-CoA carboxylase 1, Apo-B100: Apo lipoprotein B100, FASN: Fatty acid synthase, FATP4: Fatty acid transport protein 4, FBS: Fetal bovine serum; FEN: Fenofibrate, FFA: Free fatty acid, L-FABP: Liver type fatty acid binding protein, LPL: Lipoprotein lipase, MTTP: Microsomal triglyceride transfer protein, NAFLD: Non-alcoholic fatty liver disease, PBS: Phosphate buffer saline, PPAR-α: Peroxisome proliferators activator receptors alpha, RPMI: Roswell Park Memorial Institute, SIM: Simvastatin, SREBF1c: Sterol regulatory element-binding protein 1c, TG: Triglyceride, TSG: 2, 3, 5, 4-tetrahydroxy-stilbene-2-O-β-Dglucoside, VLDL: Very low density lipoprotein


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