固有免疫信号因子MyD88在CCl4致大鼠肝纤维化模型中的表达

目的观察固有免疫信号因子MyD88在肝纤维化大鼠肝脏中的表达特点,探讨MyD88与肝纤维化发生发展的关系。方法将40只SD大鼠随机分成正常对照组和实验组,以四氯化碳皮下注射和高脂低蛋白饮食复制大鼠肝纤维化模型。在制备模型实验过程中的第6个月根据不同检测目的进行取材。石蜡切片常规HE染色和免疫组化实验,另一部分标本直接进行RT-PCR实验和Western blot实验检测。结果 HE结果显示,正常组大鼠肝小叶结构罗列规则有序,未见大量炎性细胞等异构细胞出现。而MyD88在内皮细胞轻度表达,而在星形细胞并未见明显表达。模型组肝小叶结构明显破坏,数量明显减少,结构紊乱无序,代之以大量异常细胞浸润,纤维增生等特点。内皮细胞、星形细胞等MyD88都有强烈高表达,并且以胞核表达为主,亦见胞浆表达。而基因和蛋白表达都明显升高,与正常对照组相比,呈现显著性差异(P<0.01)。结论 MyD88在肝纤维化中表达显著增强,可能在纤维化形成中起到重要作用。

The expression of MyD88 in liver of CCl4-induced hepatic fibrosis mouse model

To explore the relationship between observe innate immune signaling factor MyD88 and hepatic fibrosis,we observed the expression of MyD88 on hepatic cell,and its gene and protein expression pattern in hepatic fibrosis rat.Total of 40 SD rats were randomly divided into control group and model group.Rat model of hepatic fibrosis was prepared by subcutaneous injection of carbon tetrachloride.We collected specimen in the 6 th month of model experiment in the preparation for Paraffin HE staining,and immunohistochemistry experiments,RT-PCR,and Western blot experiment.The HE result showed that the hepatic lobular structure of model group rats were significantly damaged,dramatically decrease in the amount,structure disordered,and characterized with a large number of abnormal cells infiltration,fiber and hyperplasia.Furthermore,in medal group,MyD88 in endothelial cells and stellate cells had a strong high expression,mainly on nucleus,also could be seen in cytoplasm.Compared with normal control group,the gene and protein expression in model group were significantly increased(P < 0.01).All results suggest that MyD88 expression in rats with hepatic fibrosis is significantly enhanced,which probably closely relate with fibrosis formation.