摘要
目的观察异丙酚对全脑缺血再灌注大鼠易损区海马CA1区NMDAR1表达的影响,探讨异丙酚脑保护作用机制。方法采用Pulsinelli-Brierley四血管阻断法制备全脑缺血模型。雄性Wistar大鼠50只,随机分为A组(假手术组)、B组(缺血再灌注对照组)、C组(异丙酚处理组)。C组按异丙酚剂量又分为C1组(50mg·kg-1)、C2组(100mg·kg-1)、C3组(150mg·kg-1)3个亚组。于全脑缺血15min再灌注3h后灌流固定断头取脑,采用免疫组织化学方法,检测缺血再灌注后海马CA1区NMDAR1蛋白表达。结果各组与缺血再灌注对照组比较,大鼠海马CA1区NMDAR1积分光密度、阳性细胞面积、平均灰度值均存在显著性差异(P<0.05或0.01)。结论异丙酚对缺血再灌注脑组织具有保护作用,其作用机制之一可能是与抑制NMDAR蛋白表达有关。
Aim To investigate the effect of propofol on NMDAR1 expression in hippocampus CA1 with global cerebral ischemia - reperfusion rats. Methods Fifty male Wistar rats were randomly allocated to five groups; group A received sham operation, group B ischemia - reperfusion, and group C propofol 50mg·kg^-1 ( C1 ) or 100 mg·kg^-1 (C2) or 150mg·kg^-1 (C3) before ischemia- reperfusion. Global cerebral ischemia was induced by tightening the suture for 15 min which was then loosened for reperfusion. After 3h reperfusion, the animals were decapitated on ice and the brains were immediately removed. The NMDAR1 expression was detected using immunohistochemistry method. Results The integrated OD total, average gray value and threshold area of NMDAR1 expression in Group C1 - 3 were higher than those of group B ( P 〈 0.05 or 0.01). Conclusion Propofol has protective effect in hippocampus CA1 with global cerebral ischemia- reperfusion. The protective mechanism might be involved in inhibiting NMDA receptor expression.
出处
《解放军药学学报》
CAS
2005年第6期423-426,共4页
Pharmaceutical Journal of Chinese People's Liberation Army
关键词
异丙酚
缺血再灌注
NMDAR
海马
Propofol
Ischemia - reperfusion
N - methyl - D - aspartate receptor
Hippocampus