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目的研究重复经颅磁刺激(rTMS)对脑梗死大鼠神经功能恢复及梗死侧皮质内源性神经干细胞激活、增殖的影响。方法将72只雄性SD大鼠随机分为模型组、假刺激组、rTMS组,每组24只,各组根据脑梗死后不同时间点再分为1、7、14、21 d四个亚组,每个亚组6只。采用线栓法制作左侧大脑中动脉闭塞脑梗死模型。rTMS组于动物清醒后当天即给予每天2次、每次30个脉冲的rTMS治疗(频率为0.5 Hz,场强为1.33 T);假刺激组模拟rTMS固定大鼠头部放置线圈但不给予脉冲磁刺激;模型组不给任何治疗。各组在规定的时间点应用改良的神经功能缺损评分(mNSS)进行神经功能评定,治疗结束前24 h腹腔注射5-溴脱氧尿嘧啶核苷(BrdU),应用免疫组织化学技术检测梗死侧皮质巢蛋白(nestin)及BrdU表达阳性细胞的数量。结果 rTMS组脑梗死后7、14、21 d mNSS评分明显低于假刺激组及模型组同时间点大鼠(P<0.05),假刺激组及模型组大鼠脑梗死后不同时间点mNSS评分差异不明显(P>0.05)。脑梗死后1d模型组、假刺激组和rTMS组梗死灶周围皮质均可见nestin及BrdU阳性细胞,7 d达高峰。和假刺激组及模型组同时间点相比,rTMS组7、14、21 d nestin及BrdU阳性细胞数量明显增多,两者比较差异明显(P<0.05)。结论 rTMS能促进脑梗死大鼠神经功能恢复,机制可能与rTMS治疗能促进脑梗死周围内源性神经干细胞的激活及增殖有关。
Objective To study the effects of rTMS on the recovery of neurological function and the activation and proliferation of endogenous neural stem cells in infarcted cortex in rats after cerebral infarction. Methods Seventy-two male Sprague-Dawley rats were randomly divided into model group, sham stimulation group and rTMS group, 24 rats in each group. Each group was subdivided into four sub-groups according to different time points after cerebral infarction: 1,7,14,21 days , 6 in each subgroup. The left middle cerebral artery occlusion cerebral infarction model was made by the method of thread occlusion. The rTMS group was given twice-daily rTMS treatment (0.5 Hz, field strength 1.33 T) twice a day on days after wakefulness in animals; the rTMS-fixed rats were placed in the sham-operated group without impulse stimulation Magnetic stimulation; model group did not give any treatment. The neurological deficits (mNSS) were assessed by neurological deficit scores (mNSS) at the prescribed time points. Intraperitoneal injection of 5 - bromodeoxyuridine (BrdU) 24 h before the end of treatment was performed. The infarct cortex was detected by immunohistochemistry Nestin and BrdU positive cells. Results The mNSS scores at 7, 14 and 21 days after cerebral infarction in rTMS group were significantly lower than those in sham-stimulation group and model group (P <0.05). The mNSS scores at different time points in sham stimulation group and model group The difference was not significant (P> 0.05). The nestin and BrdU positive cells were observed on the 1th day after cerebral infarction in model group, sham stimulation group and rTMS group. The numbers of nestin and BrdU positive cells in rTMS group increased significantly at 7, 14, and 21 days after rTMS stimulation compared with those in sham stimulation group and model group at the same time points (P <0.05). Conclusion rTMS can promote the recovery of neural function in rats with cerebral infarction. The mechanism may be related to the rTMS treatment can promote the activation and proliferation of endogenous neural stem cells around cerebral infarction.