核因子—κB(NF—κB)在大鼠局灶性脑缺血耐受产生中的意义

The role of NF KB in focal Cerebral ischemic tolerance Oin rats

目的:通过观察局灶脑缺血预处理对核因子κB(nuclear factor—κB,NF—κB)表达的影响初步探讨其在脑缺血耐受中的意义。方法:SD大鼠随机分为三组,对照组给予两次相前3天的假手术,其余两组分别在2小时大脑中动脉缺血(MCAO)及22小时再灌注前3天给予10分钟的预缺血或假手术,比较各组梗死体积、组织病理变化及NF—κB的表达。结果:预缺血组梗死体积较假手术组减小53.15％(p〈0.01),神经元损伤、坏死轻于后者,NF—κB表达低于假手术组及对照组(p〈0.01)。结论:10分钟大脑中动脉预缺血可有效诱导缺血耐受,减小梗死体积,减轻缺血性神经损伤,抑制NF—κB表达。NF—κB表达下调可能是局灶性脑缺血耐受产生的分子机制之一。

Objective: Investigate the expression of nuclear factor - kB (NF - kB ) in ischemic tolerance induced by focal ischemic preconditioning in rats. Method; 32 rats were divided into 3 groups in which control group received sham surgery (SS) only , and the other two groups received 2 hours of middle cerebral artery occlusion (MCAO) followed by 22 hours of reperfusion with or without 10 mintues of ischemic preconditioning (PC) 3 days before. Infarct volume , HE staining and NF -kB immunoreactivity were evaluated in each group. Results: Compared with the SS group, there was a smaller infarct volume, less severe neuronal injury and lower NF - KB immunoreactivity in PC group . Conclusion: lOminutes of ischemic PC was strong enough to induce ischemic tolerance and inhibit activation of NF - KB . Down - regulation of NF - KB might play an important role in the molecular mechanism of cerebral ischemic tolerance induced by focal ischemic preconditioning.