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核转录因子-κB在FK506保护肝脏缺血再灌注损伤中的作用 被引量:2

The central role of NF-κB in FK506 protecting liver from ischemia/reperfusion injury in rats
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摘要 目的 研究FK5 0 6能否抑制缺血再灌注损伤肝脏核转录因子 κB(NF κB)的结合活性。方法 采用大鼠部分肝血供被阻断的缺血再灌注损伤模型 ,左半肝缺血 90min ,再灌注分 0、30min ,1、2、4h等时点。实验组术前静脉注射FK5 0 6 ( 0 .3mg/kg体重 ) ,观察对照组、缺血再灌注组及FK5 0 6处理组间肝组织中NF κB的结合活性 (凝胶滞留电泳方法 )。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结合活性较强 ,再灌注 4hNF κB结合活性减弱。FK5 0 6可以抑制NF κB与其特异性调控序列的结合活性。结论 FK5 0 6通过抑制NF κB的结合活性改善肝脏缺血再灌注损伤。 Objective To determine whether FK506 can suppress hepatic ischemia/reperfusion-induced NF-κB activation.Methods Rats underwent partial hepatic ischemia (90 min) and reperfusion (in defined time course: 0 min,30 min,1 h,2 h,4 h) with or without intravenous injections of FK506 (0.3 mg/kg).NF-κB activation was evaluated by electrophoresis mobility shift assay (EMSA).Results Hepatic NF-κB activation was induced in a time-dependent manner.NF-κB activation was strong within 1 h and 2 h after the initiation of reperfusion and then decreased after 4 h.FK506 suppressed NF-κB activation.Conclusion FK506 protects against hepatic ischemia/reperfusion injury by suppressing NF-κB activation.
出处 《中华实验外科杂志》 CAS CSCD 北大核心 2003年第3期232-233,共2页 Chinese Journal of Experimental Surgery
关键词 核转录因子—κB FK506 肝脏缺血 再灌注损伤 保护作用 NF-κB Liver Reperfusion injury
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