摘要
目的 探讨核因子 (NF) κB/I κB传导通路在肝脏缺血再灌注损伤中的作用。方法采用阻断大鼠部分肝血供的缺血再灌注损伤模型 ,左半肝缺血 90min ,再灌注分 0、1、2、4h等时点。用凝胶滞留电泳方法测定NF κB的结合活性 ;应用逆转录 聚合酶链反应 (RT PCR)测定肝组织中肿瘤坏死因子 α(TNF α)、细胞间粘附因子 1(ICAM 1)mRNA的表达量。结果 肝脏缺血再灌注损伤时NF κB与其特异性调控序列的结合活性增高且具有时相性。再灌注 1～ 2hNF κB结合活性增高 ,4h后开始降低。肝组织中TNF α、ICAM 1mRNA表达在再灌注 2h后升高。讨论 肝脏缺血再灌注损伤时 ,NF κB激活并进入细胞核内 ,与一些炎症因子基因启动子区特异序列结合 ,上调TNF α、ICAM 1mRNA表达 ,从而引起肝脏缺血再灌注损伤。
Objective To explore the role of NF-kappaB/I-kappaB pathway during ischemia reperfusion (I/R) injury of the rat liver.Methods The rats underwent partial hepatic ischemia and reperfusion.The left and median lobe of the liver were subjected to ischemia for 90 min followed by reperfusion for defined time.NF-kappaB activity was analyzed by electrophoretic mobility shift assay (EMSA).Semiquantitative reverse-transcriptase polymerase chain reaction was used to analyze TNF-α and ICAM-1 mRNA levels.Results During liver I/R injury,NF-kappaB activation was induced in a time-dependent fashion.NF-kappaB was activated within 1 h and 2 h after the initiation of reperfusion and decreased afer 4 h.mRNA expression of TNF-α and ICAM-1 was increased after the reperfusion for 2 h.Conclusion During hepatic I/R injury,NF-kappaB was activated and binded to special sequence in the promoters of budget genes,which regulated the expression of TNF-α and ICAM-1mRNA.
出处
《中华实验外科杂志》
CAS
CSCD
北大核心
2003年第7期614-615,共2页
Chinese Journal of Experimental Surgery
