N-myc下游调节基因2在七氟醚预处理减轻大鼠局灶性脑缺血再灌注损伤中的作用  

Role of N-myc downstream regulated genes 2 in attenuation of focal cerebral ischemic-reperfusin injury by sevoflurane preconditioning in rats

作　　者：李新[1] 罗鹏[2] 王枫[1] 王世全[1] 李艳 杨谦梓[1] 李旭颖[1] 王强[1] 熊利泽[1] 

机构地区：[1]第四军医大学西京医院麻醉科,西安市710032 [2]第四军医大学西京医院神经外科,西安市710032 [3]西安市妇幼保健医院麻醉科

出　　处：《中华麻醉学杂志》2011年第9期1110-1113,共4页Chinese Journal of Anesthesiology

摘　　要：目的评价N-myc下游调节基因2（NDRG2）在七氟醚预处理减轻大鼠局灶性脑缺血再灌注损伤中的作用。方法健康雄性成年SD大鼠48只，体重280～320g，采用随机数字表，将大鼠随机分为3组（n=16）：假手术组（S组）、脑缺血再灌注组（I／R组）和七氟醚预处理组（Sev组）。采用大脑中动脉阻断法制备大鼠局灶性脑缺血再灌注模型。大鼠吸入2％七氟醚1h，每天1次，连续5d行七氟醚预处理。Sev组于七氟醚预处理结束后24h制备局灶性脑缺血再灌注模型。再灌注24h时行神经功能评分，随后处死大鼠，取脑组织，测定脑梗死体积百分比，采用Western Blot法测定缺血半暗带区NDRG2和活化的Caspase-3的表达，采用免疫组织荧光测定缺血半暗带区NDRG2的表达及定位。结果与s组比较，I／R组和Sev组脑梗死体积百分比升高，神经功能评分降低，脑组织缺血区半暗带NDRG2和活化的Caspase－3表达上调（P〈0．05）；与I／R组比较，Sev组脑梗死体积百分比降低，神经功能评分升高，脑组织缺血区半暗带NDRG2和活化的Caspase－3表达下调（P〈0．05）。Sev组核内NDRG2阳性染色较I／R组减浅。结论七氟醚预处理可能通过抑制脑组织NDRG2的表达、活性和细胞凋亡，从而减轻大鼠局灶性脑缺血再灌注损伤。Objective To investigate the role of N-myc downstream regulated genes 2 （NDRG2） in attenuation of focal cerebral ischemic-reperfusin injury by sevoflurane preconditioning in rats. Methods Forty-eight healthy male SD rats weighing 280-320 g were randomly divided into 3 groups （ n = 16 each） ： sham operation group （group S）, ischemia-reperfusion injury group （group I/R） and sevoflurane preconditioning group （group Sev）. Focal cerebral ischemia-reperfusion injury was induced by right middle cerebral artery occlusion （MCAO） for 120 min followed by 24 h reperfusion. In group Sev, 2.0% sevoflurane was inhaled 1 h once a day for 5 consecutive days at 24 h before MCAO. The neurologic function was evaluated at 24 h of reperfusion and than the rats were sacrificed, and the brain was removed for determination of infarct volume percentage, NDRG2 and activated Caspase-3 expression in ischemic penumbra by Western Blot and NDRG2 expression and location by immunohisto- chemistry. Results The infarct volume percentage, NDRG2 and activated Caspase-3 expression were higher, and neurologic function score was lower in groups I/R and Sev then in group S（ P 〈 0.05）. The infarct volume percentage, NDRG2 and activated Caspase-3 expression were lower, and neurologic function score was higher in group Sev then in group I/R （ P 〈 0.05 ）. The intranuclear NDRG2 positive staining was decreased in group Sev than in group I/R. Conclusion Sevoflurane preconditioning can reduce focal cerebral ischemia-reperfusion injury by inhibiting the expression and activity of NDRG2 and apoptosis in rats.

关 键 词：肿瘤抑制蛋白质类 麻醉药 吸入 缺血预处理 再灌注损伤 脑 

分 类 号：R965[医药卫生—药理学]