长程经颅磁刺激对脑梗死大鼠皮质脑源性神经营养因子表达及神经功能恢复的影响

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。

Effect of long-term transcranial magnetic stimulation on the expression of brain-derived neurotrophic factor in cortex around the infarcted focus and the recovery of neurologic function in rats with cerebral infarction

Objective To investigate the protective effect and its underlying mechanism of long-term transcranial magnetic stimulation on cerebral infarction rats so as to provide a theoretical basis for the application of TMS in the treatment and recovery of cerebral infarction. Methods A TMS group and a sham TMS group composed of 48 rats each were administered with 1 session of TMS (200 pulses) and sham TMS daily, respectively, in 3 weeks from the 2nd day after the rats were performed the right middle cerebral artery occlusion for 90 min followed by reperfusion.The recovery of neurological function, the expression of BDNF-positive cells as well as the injured brain volume were measured and compared among the groups. Results At the 2nd and 3rd weeks after treatment, neurological deficit scores of TMS group showed a significant decrease compared with that of the sham TMS group (P<0.01). On the 3rd d, 7th d, 14th d and 21st d after treatment the count of BDNF-positive cells in cortex around the infarction focus was remarkably different between the two groups (P<0.01). And in each group on 21st d there was a significant reverse correlation between count of BDNF-positive cells and the neurological deficit score (r=-0.877, P<0.01). At the 3rd week after treatment, the injured brain volume of the TMS group was significantly smaller than that of the sham TMS group (P<0.05), correlation between injured brain volume and neurological deficit score was also significant (r=0.859, P<0.01). Conclusion The long-term TMS can promote the recovery of neurological function by sustained up-regulation of the expression of BDNF positive cells as well as reducing the injured brain volume.