目的探讨电针结合重复经颅磁刺激(rTMS)对局灶性脑缺血大鼠钙结合蛋白(Calbindin-D28k)表达的影响及其治疗缺血性脑损伤的机制。方法取Wistar大鼠120只,采用线栓法制备大鼠大脑中动脉闭塞模型,随机分为正常组、模型组、电针组、rTMS组和结合组,通过免疫组化检测脑缺血后第7、14、28日3个不同时相、不同脑区Calbindin-D28k表达的变化,并观测其神经功能评分。结果电针组、rTMS组各时相及结合组第7、14日时Calbindin-D28k阳性表达均少于正常组,结合组第28日与正常组无显著差异,电针组、rTMS组、结合组各时相Calbindin-D28k阳性表达均高于模型组,结合组各时相Calbindin-D28k阳性表达均高于电针组、rTMS组。电针和结合组各时相神经功能评分均较模型组明显改善。结论电针结合rTMS对脑卒中后神经功能的恢复具有显著的促进作用,促进Calbindin-D28k蛋白的表达可能是其治疗缺血性脑卒中的机制之一。
Objective: To investigate the effects of electro-acupuncture(EA) combined with repetitive Transcranial Magnetic Stimulation(rTMS) on migration of inherent neural stem cells after focal cerebral ischemia in adult rats and to explore the mechanism of EA combined with rTMS in treating ischemic brain injury.Methods: The model of transient focal ischemia was made by the middle cerebral artery occlusion.120 Wistar rats were randomly divided into normal group,model group,EA group,rTMS group and EA combined with rTMS group.The expressions of polysiolylated neural cell adhesion molecule(PSA-NCAM) and PSA-NCAM /5-bromodeoxyuridine(BrdU) in different encephalic regions of ipsilateral hemispheres were detected by immunohistochemical staining and the neurologic impairment rating was observed at the 7th,14th and 28th d after infarction respectively.Results: The number of PSA-NCAM-positive cells and PSA-NCAM /BrdU positive cells in different encephalic regions of ipsilateral hemispheres increased at day 7 after MCAO,reached maximum at day 14 and decreased markedly at day 28.There were significant differences in EA group,rTMS group and EA + rTMS group when compared with that of model group at day 7 and 14.There were significant differences in EA + rTMS group when compared with that of EA group and rTMS group.The improvement of neural motor function was much better in EA group,rTMS group and EA + rTMS group compared with model group.The improvement were the most obvious in EA + rTMS group.Conclusion: EA combined with rTMS can promote the functional recovery after cerebral arterial thrombosis,which might be one of the important mechanisms of EA combined with rTMS in treating ischemia brain injury.