电针对脑缺血再灌注大鼠脑皮层超微结构及Nogo-A表达的影响

作者	单位
梁艳桂	广州中医药大学附属佛山市中医医院神经内科
谭峰	广州中医药大学附属佛山市中医医院神经内科
陈杰	广州中医药大学附属佛山市中医医院神经内科
王海桥	广州中医药大学附属佛山市中医医院神经内科
王学文	广州中医药大学附属佛山市中医医院神经内科
黄勋福	广州中医药大学附属佛山市中医医院神经内科
韩福兰	广州中医药大学附属佛山市中医医院神经内科

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中文摘要:

目的探讨电针对脑缺血再灌注(ischemia reperfusion,IR)大鼠不同时间点皮层超微结构及轴突再生抑制因子Nogo-A表达的影响。方法 130只雄性SD大鼠随机数字表法分为电针组(30只)、假穴位组(30只)、模型组(30只)、假手术组(30只)和空白组(10只)。电针、假穴位、模型3组采用改良的ZeaLonga法制备左侧大脑中动脉闭塞(middle cerebral artery occlusion,MCAO)模型。电针组术后选取督脉"大椎"、"百会"穴每天给予电针治疗。假穴位组术后选取督脉"大椎"、"百会"穴旁开1寸处给予电针治疗。模型组仅作MCAO缺血再灌注模型处理,假手术组仅做手术创伤,空白组不作任何处理。运用免疫组织化学染色法及透射电镜技术观察电针对IR后1、7、28d各组大鼠脑皮层缺血区细胞超微结构及Nogo-A表达的干预作用。结果电针组脑皮层缺血区神经元、胶质细胞及血脑屏障等超微结构的损伤均较假穴位组、模型组减轻。电针组大鼠脑缺血再灌注后第1、7、28d脑皮层缺血区Nogo-A的表达均低于同期假穴位组及模型组,差异有统计学意义(P<0.05),但假穴位组与模型组同期比较,差异无统计学意义(P>0.05)。结论电针对大鼠脑缺血再灌注损伤的保护作用,可能与其减轻脑细胞超微结构的损害、下调中枢神经轴突再生抑制因子Nogo-A的表达等机制密切相关。

英文摘要:

Objective To observe the effects of electroacupuncture(EA) on the expressions of Nogo-A and the ultrastructure in the cerebral cortex at different time points after the cerebral ischemia-reperfusion in rats.Methods One hundred and thirty male Sprague Dawley(SD) rats were randomly divided into the EA group(n=30),the sham-EA group(n=30),the model group(n=30),the sham-operation group(n=30),and the blank group(n=10).The modified ZeaLonga method was used to prepare the left middle cerebral artery occlusion(MCAO) model in the first three groups.After the operation Baihui(DU20) and Dazhui(DU14) were daily needled in the EA group.One inch beside Baihui(DU20) and Dazhui(DU14) were daily needled in the sham-EA group.Rats in the model group were only treated with MCAO ischemia/reperfusion.Rats in the sham-operation group only received surgical wound.No treatment was given to rats in the blank group.The ultrastructures of ischemic cells and the intervention of the Nogo-A expressions were observed using the immunohistochemical staining and the transmission electron microscope 1,7,and 28 days after EA.Results(1) In the EA group,the damage of ultrastructures of neurons,gliocytes,and blood brain barrier in the ischemic region was alleviated when compared with that of the sham-EA group and the model group.(2) On the 1st,7th and 28th day after the cerebral ischemia-reperfusion,the expressions of Nogo-A in the ischemic cortex in the EA group was lower when compared with those in the sham-EA group and the model group at the corresponding time points,showing significant difference(P<0.05).But there was no statistical difference between the sham-EA group and the model group at the same time point(P>0.05).Conclusion The mechanism of EA for protecting cerebral ischemia/reperfusion might be closely associated with alleviating the damage on the ultrastructures of brain cells,and down-regulating the expressions of Nogo-A.

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