摘要
目的:观察局灶脑缺血预处理对亲代谢型谷氨酸受体1α(metabotropicglutamatereceptor1α,mGluR1α)表达的影响并初步探讨其在脑缺血耐受中的意义。方法:SD大鼠单纯随机分为3组,对照组给予两次假手术,其余两组分别在2h大脑中动脉阻塞(MCAO)及22h再灌注前3d给予10min的预缺血或假手术,比较各组梗死体积、脑组织病理变化及mGluR1α免疫组化染色的平均光密度(MOD)和积分光密度(IOD)。结果:预缺血组梗死体积较假手术组减小53.48%(t=8.896,P=0.0006),神经元变性、坏死亦轻于假手术组,同时伴mGluR1α表达降低(PMOD=0.00021,PIOD=0.00012)。图像分析显示3组间MOD(F=359.496,P=0.00038)及IOD(F=285.167,P=0.00036)差异有显著性意义。结论:10minMCAO可有效诱导缺血耐受,减轻二次缺血所致的神经元死亡,减少mGluR1α表达。mGluR1α表达下调可能是局灶性脑缺血耐受产生的分子机制之一。
AIM:To observe the effect of focal ischemic preconditioning (IPC) on the expre ssion of metabotropic glutamate receptor1醗xpression in ischemic tolerance in rats. METHODS:Twenty-seven SD rats were randomly divided into 3 groups in which one group received twice sham surgery (SS) only as control group, and the other two groups received 2 h middle cerebral artery occlusion (MCAO) followed by 22 h re perfusion at 3 d after 10 min IPC or SS respectively. Infarct volume, pathologic al changes in brain tissue, mean optical density (MOD) and integral optical dens ity (IOD) were evaluated with HE staining. RESULTS:Compared with the SS+MCAO group, infarct volume in the IPC+MCAO grou p significantly decreased by 53.48%(t=8.896, P=0.000 6), and there were also fe wer neuronal necrosis, degeneration and lower mGluR1醗xpression in the IPC+MCA O group (PMOD=0.000 21,PIOD=0.000 12). Imaging analysis showed that there were significant differences in MOD (F=359.496,P=0.000 38)and IOD(F=285.167,P=0.00 0 36) among the three groups.
出处
《中国临床康复》
CSCD
2003年第25期3416-3417,共2页
Chinese Journal of Clinical Rehabilitation
关键词
脑缺血耐受
亲代谢型谷氨酸受体1α
缺血预处理
动物实验
Ten-minute MCAO is efficacious to induce ischemic tolerance, reduce neuronal necrosis induced by secondary ischemia and reduce mGluR1醗xpression. Down-regulation of mGluR1醡ay be one of the molecular mechanisms of induction of cerebral ischem
