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作 者:戴瑛[1] 丁新生[2] 吴祖舜[1] 高俊凤[1] 冯美江[1]
机构地区:[1]南京医科大学第二附属医院神经内科,江苏南京210011 [2]南京医科大学第一附属医院神经内科,江苏南京210029
出 处:《南京医科大学学报(自然科学版)》2004年第6期602-604,608,共4页Journal of Nanjing Medical University(Natural Sciences)
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。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.
分 类 号:R743[医药卫生—神经病学与精神病学]
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