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目的探讨核转录因子-κB(NF-κB)、凋亡调控蛋白Bcl-2、Bax在大鼠局灶性脑缺血预处理脑组织中的表达及意义。方法线栓法阻断SD大鼠大脑中动脉建立脑缺血预处理及脑缺血模型。TTC染色法测量脑梗死体积,免疫组织化学方法检测前脑皮质、基底核NF-κB、Bcl-2和Bax蛋白的表达。结果与缺血组相比,预处理缺血组脑梗死体积明显减小(p<0.01),NF-κB蛋白和Bax蛋白表达的细胞数减少(p<0.001),Bcl-2蛋白表达细胞数明显增加(p<0.001)。结论缺血预处理可有效抑制NF-κB的激活并减少神经元的凋亡,Bcl-2蛋白表达增加和Bax蛋白表达下降可能是缺血预处理产生耐受的原因之一。
Objective To investigate the expression and significance of nuclear factor-κB (NF-κB) and Bcl-2 and Bax in rats with focal cerebral ischemic preconditioning. Methods The occlusion of middle cerebral artery of middle cerebral artery occlusion in rats by thread occlusion was performed to establish a model of cerebral ischemic preconditioning and cerebral ischemia. The volume of cerebral infarction was measured by TTC staining. The expressions of NF-κB, Bcl-2 and Bax proteins in forebrain cortex and basal nucleus were detected by immunohistochemistry. Results Compared with ischemic group, the volume of cerebral infarction in ischemic group decreased significantly (p <0.01), the number of NF-κB and Bax decreased (p <0.001), the number of Bcl-2 expressed Significantly increased (p <0.001). Conclusion Ischemic preconditioning can effectively inhibit the activation of NF-κB and decrease the apoptosis of neurons. Increased expression of Bcl-2 protein and decreased expression of Bax may be one of the causes of ischemic preconditioning.