中文摘要：

目的探讨氧化槐定碱（OSR）对小鼠脑缺血再灌注损伤的保护作用及其可能的作用机制。方法将ICR小鼠60只随机分为假手术组、模型组、OSR（62．5、125、250mg·kg-1）组、尼莫地平（6mg·kg-1）组，OSR组和尼莫地平组造模前预防性给药5d、缺血前1h及缺血再灌注后12h再分别给药1次，假手术组和模型组给予相同体积的生理盐水，各实验组除尼莫地平组灌胃外，其他各组均腹腔注射，末次给药后1h，采用线栓法构建小鼠大脑中动脉阻塞局灶性脑缺血再灌注损伤模型。利用干湿重法测定小鼠脑缺血再灌注损伤侧脑组织的含水量，计算脑指数。利用实时定量RT—PCR、Westernblot法检测小鼠脑缺血再灌注损伤侧脑组织皮层中NMDA受体NR，亚基mRNA和蛋白的表达。结果与模型组比较，OSR（62．5、125、250mg·kg-1）组和尼莫地平组可明显降低小鼠脑缺血再灌注损伤侧脑组织的含水量（P〈0．01）；OSR（125、250mg·kg-1）组和尼莫地平组可显著降低小鼠脑缺血再灌注损伤侧脑组织的脑指数（P〈0．05，P〈0．01）。与模型组比较，OSR（250mg·kg-1）组和尼莫地平组能明显抑制小鼠脑缺血再灌注损伤侧脑组织皮层NMDA受体NR，亚基mRNA和蛋白的表达（P〈0．01）。结论OSR对小鼠脑缺血再灌注损伤有良好的保护作用，其作用机制可能与抑制NMDA受体NR1亚基表达有关。

英文摘要：

OBJECTIVE To investigate the protective effects of oxysophoridine （OSR） on cerebral ischemia and reperfusion injury （CIRI） in mice and to explore its possible protective mechanism. METHODS The CIRI model of mice was induced with an 6/0 nylon monofilament coated with silicone hardener mixture via the internal carotid artery. Brain water content was determined by dry/wet weight method and the cerebral index was counted in mice. The expression of NMDA NRI mRNA and the expression of NMDA NR1 pro- tein were tested with the method of Real - time RT - PCR and Western blot in mice. RESULTS Compared with the model group, OSR （62.5,125,250 mg-kg-1 ） and nimodipine（6 mg.kg-j ） reduced the brain water content（ P 〈 0.01 ）. OSR（ 125,250 mg-kg-1 ） and nimodipine（6 mg. kg-1 ） reduced the cerebral index （ P 〈 0. 05, P 〈 0.01 ）. mRNA and protein expression of NMDA NRl were decreased by OSR （ 250 nag. kg - 1 ） and nimodipine （ 6 mg. kg - 1 ） （ p 〈 0.01 ）. CONCLUSION OSR has significantly protective effects of CIRI in mice,the effective mechanism of OSR might relate to inhibit the expression of NMDA NRi receptor.