摘要
目的 研究 Bcl- 2、Bax及海马锥体细胞形态在全脑缺血再灌注后的表达及全身亚低温对其表达变化的影响 ,探讨亚低温脑保护作用的机制。方法 采用四血管阻断法制作大鼠全脑缺血再灌注模型 ,分别进行 Bcl-2、Bax免疫组织化学及 H- E染色。结果 与常温组相比 ,全身亚低温组死亡细胞数明显减少 (P<0 .0 1) ;Bcl- 2蛋白免疫反应强度峰值增高 ,持续时间延长 ;Bax蛋白免疫反应强度峰值减低 ,持续时间缩短。结论 33℃全身亚低温并持续 4 h,对缺血性锥体细胞损害有较好的保护作用。增强 Bcl- 2蛋白的表达 ,延长其表达持续时间 ,而减弱 Bax表达 ,同时缩短其表达持续时间 ,可能是亚低温保护缺血性脑组织损害的分子机制之一。
Objective This study was designed to investigate the expression of Bcl-2 and Bax in the hippocampus and the influence of general mild hypothermia on them after ischemia-reperfusion and to probe the possible protective mechanism of mild hypothermia. Methods Transient(15min) global cerebral ischemia was induced by the four-vessel occlusion method invented by Pulsinelli. H-E staining and immunohistochemical reactions of Bax and Bcl-2 were carried out correspondingly. Results Mild hypothermia could decrease the hippocampal pyramidal cells loss and the immunoreactivity of Bax but increase the immunoreactivity of Bcl-2 in the CA 1 subfield of hippocampus. Conclusion Gerenal mild hypothermia of 33℃ lasting for 4h can protect the hippocampal pyramidal cells from ischemic damage significantly. It may be one of the mechanisms that general mild hypothermia can increase Bcl-2 immunoreactivity but decrease Bax immunoreactivity.
出处
《中风与神经疾病杂志》
CAS
CSCD
北大核心
2003年第5期418-421,共4页
Journal of Apoplexy and Nervous Diseases
基金
江苏省教委重点实验室开放课题基金资助项目 (K:990 3 8)
