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  4. Effect of silymarin on lipid and alcohol metabolism in mice following long-term alcohol consumption
 
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Effect of silymarin on lipid and alcohol metabolism in mice following long-term alcohol consumption

Journal
Journal of Food Biochemistry
Journal Volume
36
Journal Issue
3
Start Page
369
End Page
377
ISSN
1745-4514
Date Issued
2012
Author(s)
CHUNG-HSI CHOU  
YI-CHEN CHEN  
MENG-CHIEH HSU  
WEI-LUN TSAI
CHIA-YI CHANG  
CHIN-HSIEN CHIU
DOI
10.1111/j.1745-4514.2011.00543.x
URI
https://scholars.lib.ntu.edu.tw/handle/123456789/734027
Abstract
ABSTRACT An alcoholic fatty liver disease was induced by feeding an ethanol diet. Eight mice per group were randomly assigned to each following group: (1) control liquid diet + 0.5 mL ddH2O; (2) control liquid diet + 150 mg silymarin/kg body weight (BW) in 0.5 mL ddH2O; (3) ethanol liquid diet + 0.5 mL ddH2O; and (4) ethanol liquid diet + 150 mg silymarin/kg BW in 0.5 mL ddH2O. The ethanol diet increased (P < 0.05) liver size and total triglyceride levels but a gavage of silymarin reduced (P < 0.05) them. Silymarin also decreased (P < 0.05) aspartate aminotransferase (AST) value, the pathogenic hepatic lipid drop and cytoplasmic vacuolization formation in alcohol-fed mice, with respect to the regulation of lipogenesis and alcohol metabolism, although silymarin did not (P < 0.05) influence 3-hydroxy-3-methylglutaryl-CoA reductase, sterol regulatory element-binding protein-1, acetyl-CoA carboxylase, fatty acid synthase, carnitine palmitoyltransferase 1A (CPT1A), alcohol dehydrogenase 1 and alcohol dehydrogenase 7 gene expressions. However, proliferator-activated receptor-alpha, cytochrome P450, family 1, subfamily e, polypeptide 1, cytochrome P450, family 1, subfamily a, polypeptide 1 and catalase were up-regulated in the livers of alcohol-fed mice with a gavage of silymarin. PRACTICAL APPLICATIONS Hepatoprotection by silymarin has been attributed mainly to its antioxidant properties. Alcoholic fatty liver disease was induced by feeding mice an ethanol diet. Following co-treatment of mice with silymarin and alcohol, serum biochemical values, lipid and alcohol metabolism-related gene expression levels, as well as histopathological analyses of mice were examined. Our results demonstrate the hepatoprotective ability of silymarin against alcohol-induced liver damage in mice. The protective mechanisms of silymarin during alcohol-induced steatosis mainly result from increased energy expenditure as well as accelerated alcohol metabolism, not only from antioxidant properties in the previous literatures. This study offers another aspect of scientific evidence for silymarin on development of hepatoprotective agents.
Type
journal article

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