泄浊化瘀方对非酒精性脂肪肝大鼠肝细胞色素P450ⅡE_1表达及脂质过氧化的影响

XIEZHOU HUAYU PRESCRIPTION ON LIVER PIGMENT P450ⅡE_1 EXPRESSION AND LIPID PEROXIDATION OF RATS WITH NON-ALCOHOLIC FATTY LIVER

目的:探讨泄浊化瘀方治疗非酒精性脂肪肝的作用机制。方法:采用高脂饮食诱导大鼠非酒精性脂肪肝模型,实验分为脂肪肝模型组,泄浊化瘀方高、中、低剂量组,凯西莱对照组和正常对照组共6组。观察各组大鼠肝组织MDA含量,SOD活性,GSH含量,脂质代谢以及肝组织形态学的变化,免疫组织化学方法观察肝细胞色素P450ⅡE1的表达。结果:泄浊化瘀方高、中、低剂量组大鼠肝组织SOD活性、MDA含量、GSH含量与模型组相比差异均有显著性意义(P<0.05或P<0.01),各用药组大鼠脂质代谢水平与模型组相比也有明显差异(P<0.05)。组织学观察表明,高、中剂量泄浊化瘀方能明显减轻肝脏脂肪变性程度。各组肝细胞P450ⅡE1的表达与肝细胞脂肪变性程度相一致。结论:泄浊化瘀方的保肝降脂作用与其抑制脂肪肝P450 ⅡE1的表达,减轻脂质过氧化反应密切相关。

Objective:To investigate the mechanism of xiezhuo huayu prescription on non-alcoholic fatty liver from the expression of cytochrome P450ⅡE1 and oxidation-antioxidation function changes.Meothods: Using high-fat diet to induce non-alcoholic fatty liver model, the experimental rats were divided into model, xiezhuo huayu prescription high, medium and low dose groups, tiopronin control group and normal control group.To observe liver function,cholesterol (TC), triglyceride (TG) levels changes, test the content of MDA,GSH and superoxide dismutase (SOD) activity,and the histomorphological changes were observed by optical microscope;cytochrome P450Ⅱexpression was determined by immunohistochemical method.Results: To compare with model group, SOD activity and GSH content of rats' livers were significantly increased in three xiezhuo huayu prescription groups,and MDA content was decreased obviously;rats' serum TC, TG level were lowered in each treated group; histomorphological observation showed that the accumulation of lipid droplets in liver tissue was obviously in model group, while the normal group had no accumulation of lipid droplets. the fatty degeneration of liver was improved in three xiezhuo huayu prescription groups; hepatic cytochromeP450ⅡE1 expression was inhibited at different levels in each xiezhuo huayu prescription group.Conclusion: Xiezhuo huayu prescription can protect liver, which maybe by reducing liver cell lipid droplet accumulation, decreasing serum TC, TG content, improving liver function, enhancing the activity of SOD and GSH content in liver tissue and inhibiting P450ⅡE1 expression in non-alcoholic fatty liver rats.