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目的:研究早期强制性运动疗法对大鼠脑缺血再灌注损伤的保护作用及相关机制。方法:60只雄性SD大鼠随机分为假手术组(Sham)、模型组(MCAO/R)、强制性运动疗法组(CIMT),每组10只。采用线栓法制作大鼠大脑中动脉闭塞再灌注模型,缺血2h再灌注24h后进行神经功能评分,然后Sham组与MCAO/R组仅常规饲养,而CIMT组建立运动疗法模型,每天1次,连续7 d。利用TUNEL法检测细胞凋亡数量,并检测病灶区脑匀浆上清中超氧化物歧化酶(SOD)活性、丙二醛(MDA)含量、还原型谷胱甘肽含量(GSH)、一氧化氮合酶(NOS)活性。结果:与Sham组比较,MCAO/R组神经功能评分显著升高(P<0.001),凋亡细胞数量显著增多(P<0.001),SOD活性和GSH含量显著减少(P<0.001),MDA含量、总NOS(TNOS)、诱导型NOS(iNOS)、构建型NOS(cNOS)活性均显著升高(P<0.01或P<0.001);与MCAO/R组比较,CIMT组神经功能评分均显著改善(P<0.001),凋亡细胞数量均显著减少(P<0.001),SOD活性和GSH含量均显著升高(P<0.001),MDA含量、TNOS、i-NOS、cNOS活性均显著降低(P<0.01或P<0.001)。结论:早期CIMT可通过改善神经功能得分,抑制神经细胞大量凋亡从而起到保护MCAO/R模型大鼠的效果,其机制可能与CIMT的清除氧自由基,增强机体抗氧化能力,减轻脑缺血再灌注所致的氧化性损伤及抑制NOS尤其是iNOS介导的NO生成有关。
Objective: To study the protective effect and mechanism of early forced exercise therapy on cerebral ischemia-reperfusion injury in rats. Methods: Sixty male Sprague-Dawley rats were randomly divided into sham operation group, model group (MCAO / R), and mandatory exercise therapy group (CIMT). The model of middle cerebral artery occlusion and reperfusion was established by the method of thread occlusion. Neurological function was evaluated after 2h of ischemia and 24h of reperfusion, and then Sham group and MCAO / R group were fed only routinely. CIMT group was established once a day For 7 days. The number of apoptotic cells was detected by TUNEL method and the activities of superoxide dismutase (SOD), malondialdehyde (MDA), reduced glutathione (GSH), nitric oxide Synthase (NOS) activity. Results: Compared with Sham group, the neurological scores of MCAO / R group were significantly increased (P <0.001), the number of apoptotic cells was significantly increased (P <0.001), the activity of SOD and the content of GSH were significantly decreased (P <0.001) , Total NOS (TNOS), iNOS and cNOS were significantly increased (P <0.01 or P <0.001). Compared with MCAO / R group, neurological scores of CIMT group were significantly improved (P <0.001), the number of apoptotic cells was significantly decreased (P <0.001), the activity of SOD and the content of GSH were significantly increased (P <0.001), while the contents of MDA, TNOS, iNOS and cNOS were significantly decreased <0.01 or P <0.001). Conclusion: Early CIMT can improve the neurological function scores and inhibit the apoptosis of nerve cells in order to protect the MCAO / R model rats. The mechanism may be related to CIMT scavenging oxygen free radicals, enhance the body’s antioxidant capacity, reduce brain defects Oxidative damage induced by blood reperfusion and the inhibition of NOS, especially iNOS-mediated NO production.