摘要
目的 研究脑缺血再灌注后全身亚低温的脑保护作用及其对Bcl- 2、Bax表达的动态影响。方法 12 6只S -D雄性大鼠随机分为假手术组、常温组和亚低温组。采用Pulsinelli四血管阻断法制作大鼠全脑缺血再灌注模型 ,即刻全身亚低温 4h ,分别在 7个时间点取脑标本 ,进行Bcl- 2、Bax免疫组织化学及苏木精 -伊红染色。结果 与常温组相比 :亚低温组海马CA1区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 全身亚低温对缺血再灌注锥体细胞损害有较好的保护作用。可增强具有抗凋亡的Bcl- 2蛋白的表达 ,延长其表达持续时间 ;而减弱具有促凋亡的Bax表达 ,同时缩短其表达持续时间。此可能是亚低温对缺血再灌注脑组织损害产生保护作用的分子机制之一。
Objective To probe into the relationship between the protective effect of mild hypothermia and the expression of Bcl-2 and Bax in the hippocampus.?Methods Transient (15 min) global cerebral ischemia was induced by the four-vessel occlusion method of Pulsinelli. The hippocampal specimens were examined after H-E staining and immunohistochemical reactions for Bax and Bcl-2.?Results Mild hypothermia decreased the loss of hippocampal pyramidal cells, enhanced the immunoreactivity of Bcl-2 in the CA1 subfield of hippocampus and prolonged the expression time. But it depressed the immunoreactivity of Bax in the CA1 subfield and shortened its expression time.?Conclusion Immediate general mild hypothermia following ischemia-reperfusion for 4 h protects the hippocampal pyramidal cells from ischemic damage significantly, and this protection may be related to the upregulation of antiapoptotic protein (Bcl-2) and the simultaneous downregulation of proapoptotic protein (Bax).
出处
《徐州医学院学报》
CAS
2003年第5期391-395,共5页
Acta Academiae Medicinae Xuzhou
基金
江苏省教育厅麻醉学重点实验室开放课题基金资助项目(K990 38)
