摘要
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 study the function of apoptosis-blocking proteins Bcl-2 and Bcl-xl in the neuroprotective role of ischemic preconditioning (IPC).Methods Using the model of 4-vessel occlusion and repassing, the histopathological changes, the percentage of apoptosis and the expression of Bcl-2 and Bcl-xl proteins of the neurons in CA1 region of rat hippocampus with IPC were examined with Nissl staining, flow cytometry(FCM) and immunohistochemistry technique. Results Forebrain ischemia and reperfusin caused apoptosis of neurons in CA1 region of hippocampus; IPC protects the neurous againt the lethal ischemia/reperfusion injury by decreasing the number of apoptotic neurons; in the early period reperfusin, the expressions of Bcl_2 and Bcl_xl are induced by IPC. Conclusion Blocking the process of neuronal apoptosis after ischemic reperfusion may play an important role in the mechanism of neuroprotection induced by IPC.
出处
《中国微循环》
2000年第4期204-207,共4页
Journal of Chinese Microcirculation
基金
山东省自然科学基金!资助项目(NoY97C08044)
