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尼莫地平对沙土鼠脑缺血后细胞凋亡及Bcl-2的影响
引用本文:戴瑛,丁新生,吴祖舜,高俊凤,冯美江.尼莫地平对沙土鼠脑缺血后细胞凋亡及Bcl-2的影响[J].南京医科大学学报,2004,24(6):602-605.
作者姓名:戴瑛  丁新生  吴祖舜  高俊凤  冯美江
作者单位:南京医科大学第二附属医院神经内科 江苏南京210011 (戴瑛,吴祖舜,高俊凤),南京医科大学第一附属医院神经内科 江苏南京210029 (丁新生),南京医科大学第二附属医院神经内科 江苏南京210011(冯美江)
摘    要:目的:探讨沙土鼠短暂脑缺血后海马区细胞凋亡与Bcl鄄2表达的改变及尼莫地平的影响。方法:52只健康沙土鼠随机分成3组,假手术组(n=12),尼莫地平组(n=20),对照组(n=20)。采用夹闭双侧颈总动脉制成全脑缺血模型。尼莫地平组及对照组均夹闭双侧颈总动脉5min,随即分别予尼莫地平注射液(1mg/kg)及等量生理盐水腹腔注射。3组分别于再灌注24、48、72、168h断头取脑,海马石蜡切片,原位末端标记法(TUNEL)测定海马CA1区锥体细胞凋亡阳性数及免疫组化法测定Bcl鄄2反应强度。结果:对照组72h见大量凋亡细胞;Bcl鄄2在72h表达最强,168h明显减少。尼莫地平组凋亡细胞数明显减少(P<0.01),Bcl鄄2在24、48、72、168h均有较强表达(P<0.01)。结论:尼莫地平可显著减少沙土鼠脑缺血后海马CA1区细胞凋亡的发生,并可增强Bcl鄄2的表达;脑缺血后及时应用尼莫地平治疗具有明显脑保护作用。

关 键 词:脑缺血  细胞凋亡  Bcl—2  尼莫地平
文章编号:1007-4368(2004)06-0602-04
修稿时间:2004年3月22日

Effects of Nimodipine on Neuronal Apoptosis and the Expression of Bcl-2 after Global Cerebral Ischemia in Gerbils
DAI Ying,DING Xing-sheng,WU Zu-shun,GAO Jun-feng,FENG Mei-jiang.Effects of Nimodipine on Neuronal Apoptosis and the Expression of Bcl-2 after Global Cerebral Ischemia in Gerbils[J].Acta Universitatis Medicinalis Nanjing,2004,24(6):602-605.
Authors:DAI Ying  DING Xing-sheng  WU Zu-shun  GAO Jun-feng  FENG Mei-jiang
Institution:DAI Ying,DING Xing-sheng1,WU Zu-shun,GAO Jun-feng,FENG Mei-jiang
Abstract:Objective: To investigate the relationship between the expression of Bcl-2 and neuronal apoptosis in the gerbils hippocampus during reperfusion after cerebral inchemia and the effects of Nomodipine on it. Methods: Fifty-two gerbils were divided randomly into three groups: sham operative group(n=12), control group(n=20), nimodipion group(n=20). The cerebral ischemia was induced by occlusion of bilateral common carotid arteries. Nimodipion group and control group were given a 5 min ischemia then given Nimodipine(1 mg/kg) and NS. Three groups were reperfused at 24,48,72 and 168 h respectively. Apoptotic cells were detected by TUNEL technique. The expression of Bcl-2 was detected by immunocytochemistry technique. Results: In Control group,the levels of Bcl-2 and the number of apoptotic cells in CA1 hippocampus neurons were increased after 72 h and decreased after 168 h. In Nimodipion group, the number of apoptotic cells was reduced evidently(P < 0.01). The levels of Bcl-2 were increased after 24 h and lasted for 168 h. Conclusion: Nimodipine can reduce apoptosis occurrence and increase the expression of Bcl-2 protein after global cerebral ischemia in gerbils. The timely making use of Nimodipine after cerebral ischemia can play a role in neuroprotection.
Keywords:cerebral ischemia  apoptosis  Bcl-2  nimodipine
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