论文部分内容阅读
目的探讨凋亡抑制基因Bcl -2及Bcl-xl在缺血预处理 (IPC)对海马CA1 区神经元细胞保护中的作用。方法利用大鼠四血管阻断及再通建立前脑缺血再灌注损伤模型 ,采用尼氏染色光镜观察、流式细胞术、免疫组织化学等技术 ,观察缺血预处理海马CA1 区神经元病理组织学改变、细胞凋亡百分率及Bcl-2及Bcl -xl蛋白表达的情况。结果1、大鼠前脑缺血再灌注引起海马CA1 区部分神经元发生凋亡。2、IPC可明显地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。3、IPC可诱导缺血再灌注损伤早期缺血敏感神经元中Bcl-2和Bcl-xl蛋白表达。结论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。
Objective To investigate the effect of apoptosis-inhibiting genes Bcl-2 and Bcl-xl on neuronal cell protection in hippocampal CA1 subfields after ischemic preconditioning (IPC). Methods The model of forebrain ischemia-reperfusion injury was established by occlusion of the four vessels in rats and reperfusion. Nissl staining, flow cytometry and immunohistochemistry were used to observe the effects of ischemic preconditioning on hippocampal CA1 neurons Histological changes, the percentage of apoptosis and Bcl-2 and Bcl-xl protein expression. Results1. The forebrain ischemia-reperfusion in rat induced apoptosis of some neurons in hippocampal CA1 region. IPC can significantly reduce the number of neurons apoptosis after ischemia-reperfusion injury, resulting in cell protection. IPC can induce the expression of Bcl-2 and Bcl-xl protein in ischemic sensitive neurons during early ischemia-reperfusion injury. Conclusion Inhibition of neuronal apoptosis may be one of the protective mechanisms of IPC on cerebral ischemia-reperfusion injury.