Silymarin's Protective Effects and Possible Mechanisms on Alcoholic Fatty Liver for Rats

脂肪肝 肝损伤 化学 甘油三酯 谷胱甘肽过氧化物酶 丙二醛 超氧化物歧化酶 脂肪性肝炎 谷胱甘肽 酒精性脂肪肝 脂质过氧化 酒精性肝病 药理学 内科学 生物化学 抗氧化剂 医学 胆固醇 肝硬化 疾病
作者
Wei Zhang,Rutao Hong,Tulei Tian
出处
期刊:Biomolecules & Therapeutics [The Korean Society of Applied Pharmacology]
卷期号:21 (4): 264-269 被引量:77
标识
DOI:10.4062/biomolther.2013.020
摘要

Silymarin has been introduced fairly recently as a hepatoprotective agent. But its mechanisms of action still have not been well established. The aim of this study was to make alcoholic fatty liver model of rats in a short time and investigate silymarin's protective effects and possible mechanisms on alcoholic fatty liver for rats. The model of rat's alcoholic fatty liver was induced by intragastric infusion of ethanol and high-fat diet for six weeks. Histopathological changes were assessed by hematoxylin and eosin staining (HE). The activities of alanine transarninase (ALT) and aspartate aminotransferase (AST), the levels of total bilirubin (TBIL), total cholesterol (TC) and triglyceride (TG) in serum were detected with routine laboratory methods using an autoanalyzer. The activities of superoxide dismutase (SOD) and glutathione peroxidase (GPx) and the level of malondialdehyde (MDA) in liver homogenates were measured by spectrophotometry. The TG content in liver tissue was determined by spectrophotometry. The expression of nuclear factor-${\kappa}B$ (NF-${\kappa}B$), intercellular adhesion molecule-1 (ICAM-1) and interleukin-6 (IL-6) in the liver were analyzed by immunohistochemistry. Silymarin effectively protected liver from alcohol-induced injury as evidenced by improving histological damage situation, reducing ALT and AST activities and TBIL level in serum, increasing SOD and GPx activities and decreasing MDA content in liver homogenates and reducing TG content in liver tissue. Additionally, silymarin markedly downregulated the expression of NF-${\kappa}B$ p65, ICAM-1 and IL-6 in liver tissue. In conclusion, Silymarin could protect against the liver injury caused by ethanol administration. The effect may be related to alleviating lipid peroxidation and inhibiting the expression of NF-${\kappa}B$.

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