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为探讨凋亡抑制基因Bcl-2及Bcl-x1在缺血预处理(IPC)对大鼠海马CA1区神经元细胞保护中的作用,利用大鼠四血管阻断和再灌注及再通建立前脑缺血再灌注损伤模型,采用尼氏小体染色光镜观察、流式细胞术、免疫组织化学等技术,观测缺血预处理海马CA1区部分神经元病理组织学改变,细胞凋亡百分率及Bcl-2和Bcl-xl蛋白表达的情况。结果发现,大鼠前脑缺血再灌注引起海马CA1区部分神经元发生凋亡,IPC还可明显的减少缺血再灌注损伤后凋亡的神经元数目,产生细胞保护作用,IPC可诱导缺血再灌注损伤早期缺血敏感神经元中出现Bcl-2及Bcl-x1蛋白的表达。结果提示,抑制神经元凋亡发生可能是IPC对脑缺血再灌注损伤起保护作用的机制之一。
To investigate the role of apoptosis-inhibiting genes Bcl-2 and Bcl-x1 in the neuronal protection of hippocampal CA1 neurons in rats after ischemic preconditioning (IPC), we used rat occlusion and reperfusion The model of cerebral ischemia-reperfusion injury was observed by Nissl microscopy, flow cytometry and immunohistochemical techniques to observe the histopathological changes, the percentage of apoptotic cells and the percentage of apoptotic neurons in hippocampal CA1 area Bcl-2 and Bcl-xl protein expression. The results showed that forebrain ischemia-reperfusion induced apoptosis of some neurons in hippocampal CA1 region, and IPC could also significantly reduce the number of neurons apoptosis after ischemia-reperfusion injury, resulting in cytoprotective effect, IPC-induced lack of Expression of Bcl-2 and Bcl-x1 proteins in ischemic sensitive neurons during early reperfusion injury. The results suggest that inhibition of neuronal apoptosis may be IPC one of the mechanisms of cerebral ischemia-reperfusion injury.