大鼠肾缺血再灌注损伤时c-fos基因的表达  

Expression of Protooncogene c-fos in Rat Renal Ischemic Reperfusion

作　　者：程向明[1] 刘平 钟庆晨 张留保 张爱羚 周其锦 郭丹 沈爱云 赵萍 

机构地区：[1]海军414医院肾内科,南京210015 [2]海军414医院解剖学教研室 [3]海军414医院内科学教研室 [4]海军414医院病理学教研室 [5]海军414医院生理学教研室

出　　处：《海军医高专学报》1997年第4期193-196,共4页

基　　金：海后计划科研课题!97-3313

摘　　要：为探讨原癌基因c－fos在急性缺血性肾脏损伤修复中的分子调控作用，用免疫组织化学法及原位分子杂交技术，对急性肾缺血再灌注后大鼠肾组织内Fos蛋白及c－fosmRNA表达的分布、强度、时程和动力学等特征进行了研究。缺血再灌注早期即可诱导肾组织中c－fos的高效表达，肾缺血45min，Fos蛋白表达在再灌注1h、2h～4h达高峰、8h锐减、24h消失。c-fosmRNA0.5h出现、1h达高峰、2h锐减，到4h时极少。原癌基因c－fos的高效表达可能参与缺血再灌注所致肾脏损伤修复的分子调控，从而影响其病变过程。To identify changes of the regulatory molecular mechanism following renal ischemic reperfusion, the characteristics of distribution, strength, time course, and dynamics of Fosprotein and c-fos mRNA expression in rat renal ischemic reperfusion were investigated by immunohistochemistry and in situ hybridization. The expression of c-fos gene in the rat kidney increased obviously in the early stage after ischemic reperfusion. Fos protein was first induced at 1h,peaked at 2 - 4 h, decayed at 8h and disappeared at 24 h during ischemic reperfusion after 45 minrenal ischemia, while expression of c-fos mRNA appeared at 0.5 h, peaked at 1 h, decayed at 2h, and disappeared nearly at 4 h after ischemic reperfusion. The results suggested that the highexpression of protooncogene c-fos might be involved in the molecular regulation mediating renalrecovery from acute ischemic reperfusion injury. The increase of c-fos gene probably plays someroles in pathologic process of acute renal ischemic reperfusion.

关 键 词：肾 再灌注损伤 C-FOS基因 原位杂交 免疫组织化学 

分 类 号：R692.5[医药卫生—泌尿科学]