摘要
目的探索肝纤维化发生的分子机制,尤其是TIMP-1,TIMP-2的作用。方法采用免疫组化和原位杂交的方法分别测定5组肝纤维化大鼠不同治疗前后TIMP-1,TIMP-2的基因调节和蛋白表达。结果 CCl_4模型组TIMP-1,TIMP-2 mRNA及蛋白水平明显高于治疗组。正常组大鼠肝组织无一例阳性。结论 TIMP-1,TIMP-2与肝纤维化形成密切相关,软肝缩脾丸对TIMP-1,TIMP-2的基因和蛋白表达有一定的抑制作用。
AIM To investigate the molecules responsible for the invasion potential of LC by focusing on tissue inhibitor of metalloproteinase (TIMP-2 and TIMP-1), because these enzymes participate in the degradation of the extracellular matrix including the basement membrane. METHODS Normal and hepatic fibrosis liver samples were obtained from CCI_4 damaged rats underwent Rangansuopiwan treatment. Transcripts for TIMP-1 and TIMP-2 or immunohistochemical examinations were detected in the liver tissues. RESULTS In 9 of the 12 LC samples, transcripts for TIMP-1 were detected in the liver tissues, and 5 of 12 of these samples showed stronger expression in the cirrhotic tissues than in the normal tissues. On the other hand, TIMP-2 messenger RNA (mRNA) was detected in 9 of the 12 cases. The expression of TIMP-1 mRNA in CCI_4 models was significantly higher than in treatment group. It tended to have a higher ratio of TIMP-1 mRNA expression to TIMP-2 mRNA expression. Immunohistochemical examinations revealed that TIMP-1 immunoreactivity was the most intense in the CCI_4 models. CONCLUSION TIMP-1 and TIMP-2 are closely related to hepatic fibrosis in LC. Rangansuopiwan can downregulate the expression of TIMP-1 and TIMP-2.
出处
《世界华人消化杂志》
CAS
2001年第4期379-382,共4页
World Chinese Journal of Digestology
基金
河南省科委科研基金.No.96031~~
关键词
肝硬化
药物疗法
病理生理学
金属蛋白酶1组织抑制
中医药疗法
软肝缩脾丸
liver cirrhosis, experimental/drug therapy
liver cirrhosis, experimental/physiopathology
tissue-inhibitor of metalloproteinase-1/metabolism
tissue-inhibitor of metalloproteinase-2/metabolism
RNA, messenger/metabolism
