摘要
目的:研究氯胺酮对缺血再灌注脑损伤小鼠海马Bcl-2、Bax蛋白及大脑梗死体积的影响。方法:昆明纯种小白鼠共30只,随机分为4组,S组(n=7)为假手术组,C组(n=8)为缺血再灌注损伤对照组,I组(n=8)为线栓缺血梗死后氯胺酮治疗组,R组(n=7)为线栓缺血梗死再灌注后氯胺酮治疗组。结果:C组海马Bax蛋白表达明显高于其他3组(P<0.05),C组海马Bcl-2蛋白表达低于I组和R组(P<0.05)。C组脑梗死体积明显高于I组和R(P<0.05)组。C组、I组、R组的神经功能缺失体征评分无显著性差异(P>0.05)。结论:氯胺酮可降低缺血再灌注脑损伤小鼠海马凋亡基因Bax的蛋白表达和大脑梗死体积,提高抑制凋亡基因Bcl-2的蛋白表达。
Objective：To observe the effects of ketamine on Bax, Bcl-2 and volume of infarction in rat after ischemic brain damage. Methods：30 Kunming mice were randomly divided into four groups. Seven mice were undergone sham operation. In group C,eight mice were control of ischemia and reperfusion. In group Ⅰ, The right middle cerebral artery of eight mice were occluded using nylon thread embolizing and treated with ketamine while the common carotid artery were clamped. In group R, seven mice were undergone ischemia and reperfusion,and then treated with ketamine. Results ：The protein Bax of mice hippocampi in group C were more than in group Ⅰ and R,but the protein Bel-2 in group C were less than in group Ⅰ and R. The neurologic scores have no difference among C,I and R groups. The volume of infarction in group C were higher than that in group Ⅰ and group R. Conclusion：Ketamine reduce the expression of Bax in mice hippocampi through blocking Nmethyl-D-aspartate receptor,reinforce the expression of Bcl-2 which can inhibit apoptosis ,and reduce the volume of infarction following ischemie brian damage.
出处
《陕西医学杂志》
CAS
2009年第5期518-521,共4页
Shaanxi Medical Journal
基金
湖北省卫生厅医药卫生科研指导计划项目资助(No2001WZ01514)
