尼莫地平联合电针治疗脑缺血再灌注损伤的机理

目的：研究尼莫地平联合电针疗法对大鼠脑缺血再灌注的保护作用机理。方法：60大鼠随机分为3组，治疗组（24只）、对照组（24只）、正常组（12只），前两组制作脑缺血再灌注模型，治疗组给予尼莫地平联合电针处理，对照组给予生理盐水，正常组不治疗。再灌注1d,3d后检测脑组织过氧化物歧化酶（SOD）、丙二醛（MDA）的含量，以及生长相关蛋白－43（GAP－43）、微管组关蛋白－2（MAP－2）和细胞周期蛋白（cyclin)-D1的表达情况。结果：缺血再灌注后SOD活性降低，MDA含量增高，缺血性周围GAP－43、MAP－2和cyclin-D1表达增高，治疗可减轻脑损害，增强GAP－43和MAP－2表达，抑制cyclin-Dl表达。结论：尼莫地坪联合电针疗法可清除自由基，抑制细胞凋亡和蛋白水解，并促进损伤组织的再生和修复。

Therapeutic mechanism of nimodipine combined with electroacupuncture treating cerebral ischemia and reperfusion injury

ObjectiveTo study the mechanism of nimodipine combined with electroacupuncture therapeutics protecting rats from cerebral ischemia and reperfusion injury.Methods60 rats were divided randomly into 3 groups, 24 rats in treatment group that accepted nimodipine combined with electroacupuncture therapy after middle cerebral artery occlusion (MCAO) for one hour, and 24 in control group,which acceptd normal saline after ischemia and reperfusion injury, and 12 rats in normal group. One or three days later, all rats were decapitated and their brains were extracted for superoxide dismutase(SOD) activity and malonaldehyde(MDA) concentration assay. And immunohistochemistry was used to detect the expression of growth associated protein 43(GAP 43),microtubule associated protein 2(MAP 2) and cyclin D1 protein.ResultsAfter ischemia and reperfusion injury,SOD activity markedly decreased in both treatment and control group while MDA concentration increased, compared with normal group( P <0 01).Level of MAP 2 expression in treatment and control group was markedly lower than normal group( P <0 01), while levels of GAP 43 and cyclin D1 expression were higher ( P <0 01). Contrasted to control group, SOD activity was higher and MDA concentration was lower in treatment group. Level of GAP 43 and MAP 2 expression in treatment group were higher than those in control group, while level of cyclin D1 lower. Differences between treatment group and control group were significent( P <0 01).ConclusionsNimodipine combined with electroacupuncture therapeutics can prevent brains from ischemia and reperfusion injury. It's actions of wiping free radicals out, inhibiting apoptosis and protein hydrolysis and promoting nerve regeneration are involved in the mechanism.