乙醇性脂肪肝模型大鼠肝脏G蛋白表达水平的变化

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。

The quantitative variance in expression level of G protein in alcoholic fatty liver model of rat

Objective To seek for the putative mechanism of liver steatosis in alcoholic fatty liver model in rat induced by high fatty diet combined with different doses of alcohol. Methods S-D rats were treated with high fatty diet in combination with different doses of ethanol for 6 weeks to establish the model of alcoholic fatty liver in rats. By the end of the 6th week, all rats were sacrificed, the level of ALT, AST, TG, TC, HDL-C in sera was meas- ured respectively, and liver ice-sections were stained with oil red O and observed by microscope, the protein expressions of Getil, Geti2, Geti3, Gets were detected by western blot. Results serum levels of ALT, AST, TG, TC increased significantly in model groups. Oil Red O stain results demonstrated apparent fat accumulation in rat liver with alcohol treatment. When combined with high fatty diet, ethanol could significantly ameliorate the expression of Gcdl, God2, Goti3, Gas. Conclusion Ethanol with high fatty diet could successfully establish alcoholic fatty liver model in rats, and the underlied mechanism may involve G protein-related downstream signaling.