摘要
目的:研究Notch通路在肝纤维发生发展中作用及可能的分子机制。方法:Wistar大鼠40只随机分为正常对照组与病理模型组,病理模型组皮下注射四氯化碳制备肝纤维化模型。8周后将大鼠处死,取肝组织行病理HE染色评价肝纤维化程度并采用免疫组织化学法检测Notch-1蛋白、E-cadherin蛋白与TGF-β1蛋白的表达。结果:肝组织病理HE染色示肝纤维化大鼠肝脏肝细胞坏死、再生明显,胶原纤维沉积明显增加,肝实质结构紊乱。与正常对照组相比,病理模型组notch-1与TGF-β1蛋白表达明显增加,而E-cadherin蛋白的表达明显下降(P<0.01)。结论:Notch通路在大鼠肝纤维化发生发展中可能起重要作用。
Objective： To investigate the effect of Notch signaling on the progression of hepatic fibrosis in a rat model induced by CCl4.Methods： Forty healthy wistar rats were randomly divided into 2 groups： control group（n =15） and liver fibrosis group（n=25）.Experimental liver fibrosis was induced by subcutaneous injection of CCl4.At the end of 8 weeks,histopathological study of liver tissue was done with hematoxylin-eosin（HE）.Notch-1,E-cadherin and Transforming growth factor-β1（TGF-β1） in liver were examined with the immunohisochemistrical technique.Results： A significant collagen deposition,hepatocyte necrosis and rearrangement of the parenchyma were noted in liver tissue of liver fibrosis group.The expression levels of notch-1and TGF-β1 increased in model group than those in control group.The expression levels of E-cadherin increased in the model animals（P〈0.01）.Conclusions： Notch signaling play important role in the occurrence and progression of hepatic fibrosis in a rat model induced by CCl4,Notch signaling and TGF-β signaling may have many consistency in the occurrence and progression of hepatic fibrosis.
出处
《现代生物医学进展》
CAS
2012年第11期2046-2048,2098,共4页
Progress in Modern Biomedicine
