NF-kB在大鼠肝缺血再灌注损伤中的活化及意义

目的探讨NFkB在肝缺血再灌注损伤过程中的作用。方法选择健康雌性Wistar大鼠24只,随机分为手术对照组,肝缺血90min组,肝缺血90min/再灌注120min组,每组8只。常规方法观察肝脏组织学改变,检测血清酶学水平和肝组织中髓过氧化物酶(MPO)含量,采用sABC免疫组织化学方法测定肝组织中NFkB的活化程度。结果手术对照组肝组织形态正常,无NFkB活化,肝功能酶学和MPO正常水平;缺血组动物肝细胞索排列紊乱,肝小叶变形,肝细胞和内皮细胞普遍水肿变性,NFkB呈中重度活化,血清酶学和MPO水平升高(P<0.01);肝缺血/再灌注组肝组织在缺血组改变基础上合并中央区局灶性肝细胞坏死,血窦内微血栓形成,汇管区中性粒细胞浸润,NFkB活化最为明显,血清酶学和MPO升高最为显著(P<0.01)。结论肝缺血再灌注时,NFkB被活化,使中性粒细胞组织浸润,对肝脏缺血再灌注损伤病理过程起到重要的作用。

The effect of nuclear factor kappa B activities on the liver of rats after ischemic reperfusion injury

Objective To investigate the role of NF-kB acivity and neutrophils on rats after hepatic ischemic reperfusion injury.Methods Twenty four healthy Wistar rats were randomly divided into 3 groups. They were normal control group (C group),subjected to 90 minutes lobar hepatic ischemic group (I group),and 90 minutes hepatic ischemia followed by 120 minutes reperfusion group (I/R group),respectively. In addition to histological examination of the liver,plasma alane aminotransferase (ALT),aspartate aminotransferase (AST)levels were respectively measured in each group. The activity of NF-kB was determined by sABC immunohistochemistry. The activity of myeioperoxidase(MPO) in liver tissue was also determined.Results Histological damage occurred in 90 minutes hepatic ischemia and 90 minutes hepatic ischemia followed by 120 minutes reperfusion. It was characterized by hepatic arrangement turbulence,hepatic lobules distortion,congestion in liver sinusoids,hepatocyte swelling or necrosis,and neutrophils infiltration. These changes were markedly obvious in I/R group,compared to I group. Normal control group didn't have activity of NF-kB,but the activity of NF-kB was markedly increased in I/R group (P<0.01). Plasma ALT and AST levels were lower in I group,while they were significantly increased in I/R group (P<0.01). In addition,liver tissue MPO activity was markedly decreased in I group,while it significantly elevated in I/R group (P<0.01).Conclusion Nuclear factor kappa B is involved and may play an important role in liver ischemic reperfusion injury.