应力纤维、纽蛋白和粘着斑激酶对大鼠肝纤维化作用机制的研究

Mechanisms of Stress Fiber, Vinculin and FAK on Hepatic Fibrosis in Rats

目的 观察应力纤维 (stressfiber)、纽蛋白 (vinculin)和粘着斑激酶 (FAK)在实验性大鼠肝纤维化形成过程中的变化 ,探讨肌动蛋白在肝纤维化形成中的作用机制。方法 雄性SD大鼠 4 0只 ,随机分为模型组 (n =30 )和对照组 (n =10 ) ,模型组给予 6 0 %四氯化碳 (CCl4) 0 1ml/ 10 0g皮下注射 ,分别于造模后 1、 4、 8周取肝组织 ,RT PCR检测vinculin和FAK的mRNA表达 ,免疫组织化学检测vinculin的表达 ,免疫荧光检测束状肌动蛋白 (F actin)的表达 ,并和对照组比较。结果 Vinculin和FAK的mRNA、vinculin的表达较对照组明显增强。免疫荧光显示模型组F actin的表达亦较对照组增强 (P <0 0 1)。结论 肌动蛋白对肝星状细胞 (HSC)激活和肝纤维化形成具有重要的作用。

Objective To observe expression changes of stress fiber, vinculin and FAK in the formation of rat hepatic fibrosis and investigate the role of actin cytoskeleton in the formation of hepatic fibrosis. Methods Tweety male SD rats were divided into two groups randomly: model group and control group. All of rats in the model group were subjected to the subcutaneous injection of 60 % CCL 4 (0.1 ml/100 g). Liver tissues were taken out at 1st, 4th, 8th week after model establishment respectively. The mRNA expression of vinculin FAK was detected by RT-PCR, and the expression of vinculin and F-actin protein were detected by immunohistochemistry and immunofluorescence respectively. Results Compared with control group, the expression of vinculin and FAK mRNA, and vinculin and F-actin protein were significantly increased (P<0.01). Conclusion Actin cytoskeleton was important on the activation of HSC and formation of hepatic fibrosis.