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预处理对老年鼠脑缺血bcl-2表达及细胞凋亡的影响
引用本文:李虹,郑世营,张正春,葛锦峰. 预处理对老年鼠脑缺血bcl-2表达及细胞凋亡的影响[J]. 实用老年医学, 2005, 19(5): 251-252
作者姓名:李虹  郑世营  张正春  葛锦峰
作者单位:215006,江苏省苏州市,苏州大学附属第一医院
基金项目:江苏省预防医学重点课题资助项目(Y200402)
摘    要:目的观察缺血预处理对脑缺血再灌注损伤的保护作用。方法将SD老年大鼠分为2组缺血预处理10min再灌注24h再次缺血24h组(PI)及单纯缺血对照组(CI),采用尼龙线栓法制作大鼠局灶性脑缺血模型,通过免疫组化染色技术及原位末端标记技术(TUNEL)检测大鼠大脑皮质bcl-2蛋白的表达和细胞凋亡情况。结果PI组较CI组缺血皮层bcl-2蛋白表达明显增强(P<0.01)。PI组缺血皮层凋亡细胞较CI组明显减少(P<0.05)。结论缺血预处理使缺血脑组织bcl-2蛋白表达增强,抑制凋亡细胞产生,说明缺血预处理对再次脑缺血有保护作用。

关 键 词:脑缺血  缺血预处理  基因bcl-2  细胞凋亡  大鼠
文章编号:1003-9198(2005)05-0251-02
收稿时间:2005-07-18
修稿时间:2005-07-18

Effects of ischemia preconditioning on bcl-2 protein expression and cell apoptosis in elderly rats after focal cerebral ischemia injuries
LI Hong, ZHENG Shi-ying, ZHANG Zheng-chun, GE Jin-feng.. Effects of ischemia preconditioning on bcl-2 protein expression and cell apoptosis in elderly rats after focal cerebral ischemia injuries[J]. Practical Geriatrics, 2005, 19(5): 251-252
Authors:LI Hong   ZHENG Shi-ying   ZHANG Zheng-chun   GE Jin-feng.
Affiliation:Department of Geriatrics, First Affliated Hospital of Suzhou University, Suzhou 215006 China
Abstract:Objective To observe the protective effects of cerebral ischemia preconditioning on cerebral ischemic injury caused by subsequent middle cerebral artery occlusion (MCAO) in SD rats. Methods Male Sprage-Dawley rats were divided into two groups. The first group(PI): 10 minutes of ischemic precondition, 24 hours of reperfusion, and then 24 hours of occlusion of the right middle cerebral artery (MCA); the second group (CI): occlusions of MCAO were performed by inserting nylon suture into the internal carotid artery. Immunohistostaining and TUNEL staining technique were used to examine bcl-2 protein expression and neuronal apoptosis on ischemic cortex. Results In the PI group positive bcl-2 protein expression in the ischemic cortex was more notable than that in the CI group (P<0.01); Cell apoptosis in the ischemic cortex of CI group is much more than that of PI group (P<0.05). Conclusions Ischemic preconditioning increases expression of bcl-2 protein and inhibits cell apoptosis, so it may induce ischemic brain tolerance and has protective effects.
Keywords:Brain ischemia  Ischemio preconditioning  Genes   bcl-2  Apoptosis  Rats
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