脑缺血再灌流诱导神经细胞凋亡机制的探讨

STUDY OF THE MECHANISM OF NEURONAL APOPTOSIS INDUCED BY CEREBRAL ISCHEMIA-REPERFUSION

目的：研究缺血再灌流损伤时脑神经细胞凋亡的发生情况及其发病机制。方法：本实验在兔幕上脑组织缺血再灌流模型成功的基础上，分别检测正常组和缺血再灌流组动物1）脑组织匀浆中SOD、MDA、TNF、IL1及牛磺酸水平，2）血浆中TNF、IL－1水平，3）细胞凋亡的染色情况，4）电镜下病理改变。结果：缺血再灌流组较正常组出现了明显的早期细胞凋亡改变，而且氧自由基及TNF、IL-1水平明显升高。结论：证明在脑缺血再灌流时发生了明显的神经细胞凋亡，其发病机制与氧自由基及细胞因子的水平升高有关，二者都可通过直接损伤DNA和／或非染色体途径诱发细胞凋亡。

Aim: To study the mechanism of neuronal apoptosis during brain ischemia-reperfusion. Methods:The rabbit global ischemia-reperfusion model was established at first, and the animals were divided into normal control and ischemia-reperfusion groups. Levels of SOD、 MDA、TNF、 IL-1 and taurine in brain tissue were determined and levels of TNF、 IL-1 in plasma were also determined. Neuronal apoptosis was observed by dye of TUNEL and electron microscope. Results: The obvious early neuronal apoptosis was found in ischemia-reperfusion group,in which levels of oxygen free radicals and TNF and IL-1 were higher than those of normal group. Conclusion: Our study proved that the early neuronal apoptosis appeared obviously during the brain ischemia-reperfusion injury. Its mechanism was related to the increase of oxygen free radicals and cytokines, which can induce early neuronal apoptosis by injuring DNA directly and/or nonchromatic way.