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目的:探讨意向性运动疗法干预后与神经可塑性相关的信号通路。创新点:首次发现意向性运动疗法干预后信号传导与转录激活因子3(STAT3)表达增高,以及STAT3直接调控神经可塑性相关基因。方法:将大脑中动脉梗死(MCAO)模型大鼠随机分为MCAO组、环境改变组和意向性运动疗法组。18天后测量三组大鼠的脑梗死面积。应用逆转录聚合酶链反应(RT-PCR)和荧光免疫染色法分别检测STAT3的基因和蛋白的表达;应用染色质免疫共沉淀检测STAT3是否绑定脑源性神经营养因子(BDNF)、突触素以及蛋白激酶Cα相互作用蛋白1(PICK1)。结论:研究结果显示:意向性运动疗法干预15天后,STAT3的基因与蛋白均增高;STAT3绑定皮层神经元BDNF、PICK1和突触素的启动子区;意向性运动干预后STAT3的升高可能与神经可塑性相关。
Objective: To investigate the signal pathways involved in neuroplasticity after intervention of intentional exercise therapy. Innovative point: The first discovery of intention-induced exercise therapy intervention signal transducers and activators of transcription 3 (STAT3) increased, and STAT3 direct regulation of neural plasticity-related genes. Methods: Middle cerebral artery occlusion (MCAO) rats were randomly divided into MCAO group, environmental change group and intentional exercise therapy group. After 18 days, the infarct size of the three groups of rats was measured. The expression of STAT3 gene and protein was detected by reverse transcriptase-polymerase chain reaction (RT-PCR) and fluorescent immunostaining, respectively. The expression of STAT3 was detected by chromatin immunoprecipitation. BDNF, synapse And protein kinase Cα interacting protein 1 (PICK1). CONCLUSIONS: The results showed that STAT3 gene and protein were all increased after 15 days of intervention by intention-to-exercise therapy. The promoter regions of BDNF, PICK1 and synaptophysin in STAT3-bound cortical neurons might be associated with the increase of STAT3 after intentional exercise intervention Related to neural plasticity.