电针预处理对脑缺血再灌注后SOD_2的表达影响

目的观察电针预处理对脑缺血再灌注后锰超氧化物歧化酶表达的影响。方法成年雄性C57小鼠随机分为假手术组(sham)、电针预处理组(EA)、大脑中动脉栓塞组(MCAO)、电针加大脑中动脉栓塞组(EA+MCAO),采用MCAO法诱导小鼠局灶性脑缺血再灌注模型。再灌2 h应用Western blot以及免疫荧光组织化学染色技术检测SOD2表达,再灌24 h评估神经行为学、测量脑梗死容积和神经细胞凋亡。结果脑缺血再灌注2 h,SOD2表达显著降低,而电针预处理可上调SOD2的表达,增加SOD2在神经元的免疫荧光强度。同时电针预处理可改善缺血再灌注后的神经功能障碍,减轻脑梗死容积率,减少末端脱氧核苷酸转移酶介导的生物素脱氧尿嘧啶核苷酸缺口末端标记法(TUNEL)阳性细胞数目。结论电针预处理可上调脑缺血再灌注后SOD2表达,可能参与其诱导的脑保护作用。

Effect of electroacupuncture pretreatment on expression of manganese superoxide dismutase after cerebral ischemia and reperfusion in mice

Objective The effect of electroacupuncture （EA）pretreatment on the expression of manganese superoxide dismutase （SOD2） after cerebral ischemia and reperfusion is investigated.Methods Adult male C57 mice were randomly divided into 4 groups：sham,EA,middle cerebral artery occlusion （MCAO）,EA ＋MCAO.Cerebral ischemic injury was induced by transient middle cerebral artery occlusion （tMCAO） at 2 h after EA pretreatment.The expression of SOD2 was analyzed by Western blot and immuneflourescence staining at 2 h after reperfusion.At 24 h after reperfusion,the infarction volume and neurological scores were evaluated and the apoptotic cells were examined by transferase-mediated deoxyuridine triphosphate-biotin nick end labeling （TUNEL） staining.Results At 2 h after reperfusion,the expression of SOD2 in MCAO group was decreased,and EA pretreatment increased the content of SOD2 at 2 h after reperfusion compared with MCAO group.EA pretreatment improved the neurological behaviors and attenuated the infarct volume in EA ＋ MCAO group.EA pretreatment reduced the number of apoptotic cells in penumbra.Conclusion EA pretreatment increases the expression of SOD2,which may be involved in the neuroprotection induced by EA pretreatment.