摘要
目的 探讨脑缺血再灌流损伤时神经细胞凋亡及其调控基因 bcl- 2的作用。方法 采用大鼠大脑中动脉 (MCA)阻断模型阻断血流 2小时后再灌注 ,分别在不同再灌注时间将大鼠断头取脑 ,连续切片分别作 HE、TUNEL染色及 bcl- 2蛋白免疫组化染色。结果 (1) MCA阻断后脑缺血周边区部分神经细胞发生凋亡 ,随着再灌注时间的延长 ,一定时程内凋亡细胞逐渐增多 ,2 4小时达高峰 ,各组之间及与假手术组之间差异显著 (P<0 .0 1)。 (2 )凋亡抑制基因 bcl- 2在再灌注早期 (6小时 )即达高峰 ,各组大鼠 bcl- 2表达亦存在显著差异 (P<0 .0 1)。 (3)神经细胞凋亡的出现与 bcl- 2表达在一定时程内呈直线负相关 (r=- 0 .747,P<0 .0 1)。结论 脑缺血再灌流损伤时 ,神经细胞凋亡起着重要作用 ,这种作用与 bcl- 2的表达等密切相关。
Objective To investigate the effect of neuronal apoptosis and the role of its regulating gene bcl 2 in cerebral ischemic reperfusive injury. Method The middle cerebral artery (MCA) of rats was occluded for 2 h with MCAO model, and reperfusion. At each time rat brains were continuously cut to three sections for HE、TUNEL staining and bcl 2 protein immunohistochemical staining.Results 1) The number of apoptotic cells increased with the development of reperfusion within a certain time, and reached its height in 24 h. There was significant difference between each group and the sham operative group (P<0.01).2) The expression of apoptosis inhibiting gene bcl 2 reached its height at the beginning of reperfusion (6 h), and there was also a significant difference within rats bcl 2 in each group(P<0.01). 3) There was a negative correlation between the neuronal apoptosis and the expression of bcl 2 protein within a certain time(r=-0.747,P<0.01).Conclusion The neuronal apoptosis might play an important role in cerebral ischemic reperfusive injury.it correlated with the expression of bcl 2.
出处
《临床神经病学杂志》
CAS
2000年第3期134-136,共3页
Journal of Clinical Neurology
基金
安徽省教委科研基金资助!( 97JL-162 )
