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目的探讨乙醇联合高脂饮食诱导大鼠肝脏早期脂肪变性的可能机制。方法高脂饮食配合乙醇灌胃,连续6周,制备大鼠脂肪肝模型。6周末取血,检测血清丙氨酸氨基转移酶(ALT)、门冬氨酸氨基转移酶(AST)、甘油三酯(TG)、总胆固醇(TC)、高密度脂蛋白胆固醇(HDL-C);制备石蜡及冰冻切片,进行肝脏病理学检查。Westernblot分析各组大鼠肝脏组织中抑制型G蛋白α1(Gαi1)、抑制型G蛋白α2(Gαi2)、抑制型G蛋白α3(Gαi3)、刺激型G蛋白(Gαs)表达水平的改变。结果乙醇联合高脂饮食条件下大鼠血清ALT、AST、TG、TC明显升高且伴有HDL-C的显著下降;OilRedO(油红O)染色结果显示乙醇联合高脂饮食组大鼠肝脏脂肪变明显;模型组大鼠肝组织中的Gαi1、Gαi2、Gαs表达明显下降,Gαi3的表达水平在模型组中呈增高趋势。结论乙醇联合高脂饮食能够进一步诱导大鼠肝脏的脂肪变性,病变程度与乙醇剂量呈正相关,其发病机制可能和G蛋白介导的信号传导通路的改变密切相关。
Objective To investigate the possible mechanism of early fatty degeneration in rat liver induced by ethanol combined with high-fat diet. Methods High-fat diet with ethanol for 6 weeks, rat fatty liver model was prepared. Blood samples were collected at the end of 6th week to detect serum ALT, AST, TG, TC, HDL-C ); Preparation of paraffin and frozen sections for liver pathology. The expression of Gαi1, Gαi2, Gαi3 and Gαs in hepatic tissue of rats in each group were analyzed by Western blot. Results The levels of serum ALT, AST, TG and TC were significantly increased and HDL-C was significantly decreased in rats fed with ethanol and high-fat diet. OilRedO staining showed that the liver fat The expression of Gαi1, Gαi2, Gαs in the liver tissue of the model group decreased significantly, and the expression level of Gαi3 increased in the model group. Conclusions Ethanol combined with high-fat diet can further induce steatosis in rat liver. The degree of lesion is positively correlated with the dosage of ethanol. The pathogenesis may be related to the change of G protein-mediated signal transduction pathway.