摘要
目的观察转化生长因子(TGF-β)Ⅲ型受体(TβRⅢ)在二乙基亚硝胺(DEN)诱导的肝细胞癌(HCC)模型小鼠中的表达及其信号通路的变化。方法 C57BL/6J小鼠腹腔注射DEN建立HCC小鼠模型;HE染色法观察小鼠肝脏病理变化;ELISA法检测小鼠肝脏组织中TGF-β1的水平;Western blot法检测肝脏组织TβRⅢ、p-Smad2及Smad2蛋白的表达变化。结果 HE染色结果显示,对照组小鼠肝细胞大小形态正常,肝小叶结构完整,随着造模时间的延长,模型组小鼠肝小叶逐渐被破坏,肝细胞异常增生,出现病理核分裂,HCC结节形成。在DEN诱导的HCC模型小鼠中,随着造模时间的延长,肝脏TGF-β1的水平明显升高,TβRⅢ蛋白的表达降低,p-Smad2蛋白的表达升高,而Smad2蛋白的表达没有明显变化。结论 TβRⅢ表达的降低可能与HCC的发生发展有关。
Objective To detect the expression of typeⅢTGF-β receptor（ TβRⅢ） in diethylnitrosamine （ DEN）-induced liver cancer model. Methods C57BL/6J mice were intraperitoneally injected with DEN in a 20μg/g dos-age to establish liver cancer model. The pathological change of mice liver was observed by HE staining. The TGF- 〈br〉 β1 level in liver tissue was measured by ELISA assay. The expressions of TβRⅢ, p-Smad2 and Smad2 were detec-ted by Western blot. Results The mice liver cell of the control group formed normal size with the complete hepatic lobule structure. With the time passing, hepatic lobule in model group mice was destroyed gradually with liver cell dysplasia, pathology of fission, tumor nodule formation. In DEN-induced liver cancer model, the TGF-β1 level was elevated compared with the control group and the TβRⅢ protein expression was significantly decreased. The ex-pression of p-Smad2 protein was elevated, while Smad2 protein expression showed no obvious change. Conclusion The low expression of TβRⅢ may play an essential role in the progression of hepatocellular carcinoma.
出处
《安徽医科大学学报》
CAS
北大核心
2015年第7期912-916,共5页
Acta Universitatis Medicinalis Anhui
基金
国家自然科学基金(编号:81300332,81330081)
高等学校博士学科点专项科研基金(编号:20113420120002)
安徽高校省级自然科学研究项目(编号:KJ2012A153)
