Therapeutic mechanism of nimodipine combined with electroacupuncture treating cerebral ischemia and reperfusion injury
- VernacularTitle:尼莫地平联合电针治疗脑缺血再灌注损伤的机理
- Author:
Dengjun GUO
;
Wantong YANG
;
Jun TIAN
;
Ziniu DENG
;
Weijing LIAO
- Publication Type:Journal Article
- Keywords:
cerebral ischemia, reperfusion injury, electroacupuncture, nimodipine, rats
- From:
Chinese Journal of Rehabilitation Theory and Practice
2003;9(3):141-143
- CountryChina
- Language:Chinese
-
Abstract:
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.
