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作 者:徐明清[1] 薛兰[2] 龚建平[1] 韩本立[1] 董家鸿[1]
机构地区:[1]第三军医大学附属西南医院全军肝胆外科研究所、西南肝胆外科医院,重庆,400038 [2]解放军208医院,长春,130062
出 处:《第三军医大学学报》2002年第2期149-151,共3页Journal of Third Military Medical University
基 金:国家自然科学基金资助项目 (3 9970 719)
摘 要:目的 探讨缺血再灌注肝脏枯否细胞 (KCs)的活化机制。方法 Wistar大鼠随机分为肝缺血 30min再灌注组 (HIR 30min组 )、肝缺血 60min再灌注组 (HIR 60min组 )及对照组。EMSA、ELISA法检测HIR后KCsNF κB激活及KCs培养上清液TNF α含量。结果 肝缺血 30min或 60min再灌注后 0hKCsNF κB均已激活 ,NF κB活性均于HIR后 3h达到高峰 ,肝缺血时间越长 ,KCsNF κB激活越明显 ;KCs培养上清TNF α含量于HIR后 0h增高 ,HIR后 6h达到高峰 ,肝缺血时间越长 ,KCs培养上清TNF α含量越高。结论 NF κB是缺血再灌注肝脏KCs活化的关键因子。objective To study the effect of NF κB on Kupffer cells (KCs) activation during hepatic ischemia reperfusion (HIR). Methods Wistar rats were randomly divided into HIR 30 min and HIR 60 min group in which hepatic reperfusion was perforned after 30 minutes' and 60 minutes' ischemia with respectively interruption of the portal venous blood supply to liver, and sham control group in which midline laparotomy was operated without vascular occlusion. The DNA binding activity of KCs nuclear NF κB, levels of TNF α in the cultured supernatant of KCs were measured with EMSA and ELISA 0?1?3?6 and 12 h after reperfusion respectively. Results KCs NF κB was activated 0 h after reperfusion and their activity reached their peek values 3 h later, and levels of KCs NF κB activecty increased with increase of time after hepatic, reperfusion; Levels of TNF α in the cultured supernatant of KCs increased 0 h and peaked 6 h after HIR, and levels of TNF α in the cultured supernatant of KCs increased with the increase of KCs NF κB activity levels. Conclusion NF κB is the crucial factor of KCs activation during HIR.
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