Sox9在四氯化碳(CCl_(4))诱导的肝纤维化模型中的机制研究  

Study on the mechanism of sox9 in hepatic fibrosis model induced by carbon tetrachlorid

作　　者：吴钟英 周国琴 李鹏 Wu Zhongying;Zhou Guoqin;Li Peng(Guiyang Public Health Treatment Center,Guiyang 550004,Guizhou,China)

机构地区：[1]贵阳市公共卫生救治中心,贵州贵阳550004

出　　处：《贵州医药》2023年第12期1851-1853,共3页Guizhou Medical Journal

基　　金：2019年度贵阳市科技局、贵阳市公共卫生救治中心大健康科技合作项目(项目编号:[2019]9-12-3号);贵州省中医药管理局中医药、民族医药科技技术研究课题项目(编号:QZYY-2021-145);2022年度贵州省卫生健康委科学技术基金项目(项目编号:gzwkj2022-031)。

摘　　要：目的探讨sox9在四氯化碳(CCl_(4))诱导肝纤维化模型中的作用机制。方法将40只SPF级雄性C57BL/6小鼠随机分成为正常对照组(n=10)和模型组(n=30)。在模型组(n=30)的小鼠中腹腔注射四氯化碳(CCl_(4))-玉米油混合物以建立小鼠肝纤维化模型。Sox9的表达量和蛋白表达水平经由实时荧光定量PCR法、蛋白质免疫印迹法和免疫组织化学法检测。结果正常对照组和模型组均使用实时荧光定量PCR法检测Sox9在肝脏组织中的表达水平,与对照组相比Sox9的肝脏表达水平在模型组中显著提高。蛋白质免疫印迹法和免疫组织化学法检测结果均显示:与对照组相比,模型组中的Sox9蛋白质表达水平显著上调(P<0.01)。结论通过实时荧光定量PCR法、蛋白质免疫印迹法和免疫组织化学法检测发现在四氯化碳(CCl_(4))诱导小鼠肝纤维化模型中的Sox9表达量及蛋白水平均显著升高。Objective To investigate the mechanism of sox9 in hepatic fibrosis model induced by carbon tetrachloride(CCl_(4)).Methods Forty SPF male C57BL/6 mice were randomly divided into normal control group(n=10)and model group(n=30).Model group(n=30)were intraperitoneally injected with CCL4-corn oil mixture to establish hepatic fibrosis model.The expression of Sox9 was detected by real-time quantitative PCR(qRT-PCR).The protein level of Sox9 was detected by western blotting(WB)and immunohistochemistry.Results The expression level of Sox9 in liver of normal control group and fibrosis model group were detected by qRT-PCR.Compared with the normal control group,the liver expression level of Sox9 was significantly increased in the hepatic fibrosis model group.Both Immunohistochemical and WB showed that compared with the normal control group,the protein level of Sox9 in the hepatic fibrosis model group was increased.Conclusion The expression level of Sox9 in hepatic fibrosis model induced by CCl_(4) was significantly increased,which detected byqRT-PCR,WB and immunohistochemistry.

关 键 词：肝纤维化 小鼠 SOX9 

分 类 号：R575.2[医药卫生—消化系统]