延胡索乙素对大鼠脑缺血再灌注损伤的影响  

Effects of Tetrahydropalmatine on Ischemia-Reperfusion-Induced Brain Injury in Rats

作　　者：闵清[1] 李立中[1] 吴基良[1] 江翠娥[2] 王秋桂[2] 

机构地区：[1]咸宁医学院药理学教研室 [2]咸宁医学院组织胚胎学教研室

出　　处：《咸宁医学院学报》1995年第4期151-153,共3页Journal of Xianning Medical College

摘　　要：利用大鼠脑缺血再灌注损伤模型,观察延胡索乙素（THP）对脑缺血再灌注损伤的保护作用,实验结果表明,THP能使脑缺血再灌注过程中超氧化物歧化酶（SOD）活力（P<0.01）和谷胱甘肽过氧化物酶（GSHPx）活力（P<0.05）明显升高、脂质过氧化物产物丙二醛(MDA)明显下降（P<O.01）,下降了42.5％;同时使细胞膜上Na^+-K^+-ATP酶和Ca^(2+)-ATP酶活力升高（P<0.05）。结果提示,THP对脑缺血再灌注损伤有保护作用,其机理可能与抑制氧自由基及脂质过氧化物形成有关。In order to observe the protective effects of Tetrahydropalmatine (THP) on ischemia-reperfusion-induced brain injury; a model was set up by using ischemia-reperfusion induced brain injury i Rate. The date show that superoxide dismutase (SOD) activity (P&lt;0.01)and Giutathione peroxidase (GSHTX) activity (P&lt;0.05) were increased and Malondialehyde(MDA) Was decreased (P&lt;0.01) decreasing 42.5%; and the activities of Na+-K+-ATPase and Ca2+-ATPase were increased (P&lt;0.05) during brain ischemia-reperfusion. The result suggested that THP has protective effect on ischemia-reperfusion-induced brain probably by inhibiting oxygen free radicals and subsequent lipid peroxidation

关 键 词：脑缺血再灌注损伤 THP 延胡索乙素 大鼠 脂质过氧化物 保护作用 升高 制氧 产物 机理 

分 类 号：R743[医药卫生—神经病学与精神病学] R285.5[医药卫生—临床医学]