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Prevention Mechanism of 2,3,5,4’-Tetrahydroxy-stilbene-2-O-β-D-glucoside on Lipid Accumulation in Steatosis Hepatic L-02 Cell

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...

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Autores principales: Lin, Pei, Lu, Jian-Mei, Wang, Yan-Fang, Gu, Wen, Zhao, Rong-Hua, Yu, Jie
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Medknow Publications & Media Pvt Ltd 2017
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5421421/
https://www.ncbi.nlm.nih.gov/pubmed/28539716
http://dx.doi.org/10.4103/0973-1296.204563
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author Lin, Pei
Lu, Jian-Mei
Wang, Yan-Fang
Gu, Wen
Zhao, Rong-Hua
Yu, Jie
author_facet Lin, Pei
Lu, Jian-Mei
Wang, Yan-Fang
Gu, Wen
Zhao, Rong-Hua
Yu, Jie
author_sort Lin, Pei
collection PubMed
description 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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spelling pubmed-54214212017-05-24 Prevention Mechanism of 2,3,5,4’-Tetrahydroxy-stilbene-2-O-β-D-glucoside on Lipid Accumulation in Steatosis Hepatic L-02 Cell Lin, Pei Lu, Jian-Mei Wang, Yan-Fang Gu, Wen Zhao, Rong-Hua Yu, Jie Pharmacogn Mag Original Article 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. Medknow Publications & Media Pvt Ltd 2017 2017-04-18 /pmc/articles/PMC5421421/ /pubmed/28539716 http://dx.doi.org/10.4103/0973-1296.204563 Text en Copyright: © 2017 Pharmacognosy Magazine http://creativecommons.org/licenses/by-nc-sa/3.0 This is an open access article distributed under the terms of the Creative Commons Attribution-NonCommercial-ShareAlike 3.0 License, which allows others to remix, tweak, and build upon the work non-commercially, as long as the author is credited and the new creations are licensed under the identical terms.
spellingShingle Original Article
Lin, Pei
Lu, Jian-Mei
Wang, Yan-Fang
Gu, Wen
Zhao, Rong-Hua
Yu, Jie
Prevention Mechanism of 2,3,5,4’-Tetrahydroxy-stilbene-2-O-β-D-glucoside on Lipid Accumulation in Steatosis Hepatic L-02 Cell
title Prevention Mechanism of 2,3,5,4’-Tetrahydroxy-stilbene-2-O-β-D-glucoside on Lipid Accumulation in Steatosis Hepatic L-02 Cell
title_full Prevention Mechanism of 2,3,5,4’-Tetrahydroxy-stilbene-2-O-β-D-glucoside on Lipid Accumulation in Steatosis Hepatic L-02 Cell
title_fullStr Prevention Mechanism of 2,3,5,4’-Tetrahydroxy-stilbene-2-O-β-D-glucoside on Lipid Accumulation in Steatosis Hepatic L-02 Cell
title_full_unstemmed Prevention Mechanism of 2,3,5,4’-Tetrahydroxy-stilbene-2-O-β-D-glucoside on Lipid Accumulation in Steatosis Hepatic L-02 Cell
title_short Prevention Mechanism of 2,3,5,4’-Tetrahydroxy-stilbene-2-O-β-D-glucoside on Lipid Accumulation in Steatosis Hepatic L-02 Cell
title_sort prevention mechanism of 2,3,5,4’-tetrahydroxy-stilbene-2-o-β-d-glucoside on lipid accumulation in steatosis hepatic l-02 cell
topic Original Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5421421/
https://www.ncbi.nlm.nih.gov/pubmed/28539716
http://dx.doi.org/10.4103/0973-1296.204563
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