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目的探索长程经颅磁刺激(TMS)对脑梗死大鼠梗死灶周围皮质脑源性神经营养因子(BD-NF)表达和脑损伤体积、神经功能恢复的影响及作用机制,为经颅磁刺激在脑梗死治疗及康复中的应用提供理论依据。方法TMS组与假刺激组大鼠各48只,于大脑中动脉阻塞/再灌注(MCAO/R)90min后的3周内每日接受1次TMS(200脉冲)与假刺激治疗。检测2组大鼠神经功能恢复情况、梗死灶周围皮质BDNF免疫阳性细胞表达及脑损伤体积,对所得资料进行统计学分析。结果在治疗2周和3周时,TMS组神经功能缺损评分与假刺激组相比均明显降低(P<0.01)。TMS组在治疗3d、7d、14d、21d时梗死灶周围皮质BDNF阳性细胞计数与假刺激组各对应时间点相比,差异均有统计学意义(P<0.01),且2组治疗21d时梗死灶周围皮质BDNF阳性细胞计数与大鼠神经功能缺损评分呈显著负相关(r=-0.877,P<0.01)。治疗3周后,TMS组脑损伤体积明显小于假刺激组(P<0.05),2组脑损伤体积与最终神经功能缺损评分明显相关(r=0.859,P<0.01)。结论长程TMS有促进脑梗死大鼠神经功能缺损恢复的作用,其作用通过持续上调梗死灶周围皮质BDNF阳性细胞表达、减小梗死后脑损伤体积等作用而实现。
Objective To explore the effect and mechanism of long-term transcranial magnetic stimulation (TMS) on the expression of cortical BDNF, the volume of brain injury and the recovery of neurological function after cerebral infarction in rats. In the treatment and rehabilitation of cerebral infarction provide a theoretical basis. Methods Forty-eight TMS rats and sham stimulation rats received TMS (200 pulses) and sham stimulation once daily for 3 weeks after MCAO / R 90 min. The neurological function recovery, the expression of BDNF immunoreactive cells in the cortex around the infarcted area and the volume of brain injury were detected. The data were statistically analyzed. Results At 2 weeks and 3 weeks after treatment, the neurological impairment scores of TMS group were significantly lower than those of sham stimulation group (P <0.01). There were significant differences in BDNF positive cells in infarcted cortex between TMS group and control group at 3d, 7d, 14d and 21d (P <0.01), and infarction There was a significant negative correlation between BDNF positive cell count in the cortex and the neurological deficit score (r = -0.877, P <0.01). After 3 weeks of treatment, the volume of brain injury in TMS group was significantly smaller than that in sham stimulation group (P <0.05). The volume of brain injury in 2 groups was significantly correlated with the final neurological deficit score (r = 0.859, P <0.01). Conclusions Long-term TMS can promote the recovery of neurological deficits in rats with cerebral infarction. The effects of long-term TMS can be achieved by continuously up-regulating the expression of BDNF-positive cells in the cortex around infarcts and reducing the volume of brain injury after infarction.