目的 探讨运动预处理对脑缺血再灌注大鼠神经功能缺损的影响及可能机制。方法 健康Sprague-Dawley大鼠36只随机分为假手术组、模型组和运动预处理组,每组12只。后两组采用改良线栓法制备脑缺血120 min再灌注模型。再灌注2 h、12 h、24 h后,采用Longa评分法评定;再灌注24 h后,采用Western blotting检测线粒体ATP敏感性钾(mitoKATP)通道蛋白内向整流性钾离子通道6.2 (Kir6.2)和磺脲类受体1 (SUR1)的表达,TUNEL染色检测神经细胞凋亡。结果 脑缺血再灌注24 h后,与模型组比较,运动预处理组Longa评分降低(P<0.05), Kir6.2、SUR1蛋白水平下降(P<0.05),细胞凋亡减少(P<0.05)。结论 运动预处理可能通过调节mitoKATP通道蛋白表达,降低细胞凋亡,从而改善脑缺血再灌注后神经功能。
Objective To explore the effect and mechanism of exercise preconditioning on neurological deficits in rats after cerebral ischemia-reperfusion. Methods Thirty-six healthy Sprague-Dawley rats were randomly divided into sham group (n=12), model group (n=12) and exercise preconditioning group (n=12). The latter two groups were occluded middle cerebral artery for 120 minutes and reperfused with modified suture method. The rats were evaluated with Longa's score two, twelve and 24 hours after reperfusion. The expression of mitochondrial ATP-sensitive potassium (mitoKATP) channel proteins inwardly rectifying potassium channel (Kir6.2) and sulphonylurea receptor 1 (SUR1) were detected with Western blotting and the cerebral cell apoptosis was detected with TUENL assay 24 hours after reperfusion. Results Compared with the model group, the Longa's score decreased in the exercise preconditioning group 24 hours after reperfusion (P<0.05), while the expression of Kir6.2 and SUR1 decreased (P<0.05), and TUNEL-positive cells decreased (P<0.05).Conclusion Exercise preconditioning may improve neurological function after cerebral ischemia-reperfusion, which may associate with inhibiting the expression of mitoKATP channel proteins and cell apoptosis.
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