Li-Gan-Shi-Liu-Ba-Wei-San improves non-alcoholic fatty liver disease through enhancing lipid oxidation and alleviating oxidation stress

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• 作者：Youzhao Jiang^a ; Liu Chen^a ; Hui Wang^a ; Bao Narisi^b ; ; Bing Chen^a ; ^{chenbing1960@163.com" class="auth_mail" title="E-mail the corresponding author}
• 关键词：ALT ; alanine aminotransferase ; AST ; aspartate transaminase ; DMSO ; Dimethyl Sulphoxide ; FFA ; free fatty acid ; HDL-C ; high density lipoprotein cholesterol ; IκBα ; inhibitor of nuclear factor κB α ; iNOS ; inducible nitric oxide synthase ; KRP ; Krebs-Ringer phosphate ; LDL-C ; low density lipoprotein cholesterol ; LGSLBWS ; Li-Gan-Shi-Liu-Ba-Wei-San ; MDA ; malondialdehyde ; MTT ; 3-(4 ; 5-D imethylthiazol-2-yl)-2 ; 5-diphenyltetrazoliumbromide ; NAFLD ; nonalcoholic fatty liver disease ; NO ; nitric oxide ; PPAR ; pero
• 刊名：Journal of Ethnopharmacology
• 出版年：2015
• 出版时间：24 December 2015
• 年：2015
• 卷：176
• 期：Complete
• 页码：499-507
• 全文大小：5278 K

文摘

Mongolian medicine is an important constituent of traditional Chinese medicine. Its representative prescription, Li-Gan-Shi-Liu-Ba-Wei-San (LGSLBWS), is widely used for long-term treatment of chronic liver disease and nonalcoholic fatty liver disease (NAFLD).

Aim of the study

This study explored the effects and mechanism of LGSLBWS on NAFLD.

Materials and methods

NAFLD rat model was established with high-fat diet. The effects of LGSLBWS on lipid metabolism, liver function, and hepatic morphology were observed in NAFLD rats. Superoxide dismutase (SOD) and malondialdehyde (MDA) contents in the liver, as well as the expression levels of peroxisome proliferator-activated receptor (PPAR)α, PPARβ, inhibitor of nuclear factor κB α(IκBα), and inducible nitric oxide synthase (iNOS) were all detected. Finally, the effects of LGSLBWS on fatty acid oxidation, PPARα, PPARβ, IκBα, and iNOS were determined in HepG2 cells.

Results

LGSLBWS significantly reduced the fat deposition in the liver and the serum aspartate aminotransferase levels in NAFLD rats. Serum triglyceride and free fatty acid levels were reduced by LGSLBWS. Total cholesterol and triglyceride contents in the liver were also downregulated. SOD and MDA levels were increased and decreased by LGSLBWS, respectively. LGSLBWS can significantly promote fatty acid oxidation of HepG2 cells. Upregulation of PPARα, PPARβ, and IκBα and downregulation of iNOS by LGSLBWS were both observed in the NAFLD model and HepG2 cells.

Conclusions

LGSLBWS can significantly improve NAFLD by enhancing fatty acid oxidation and alleviating oxidative stress.