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首页> 美国卫生研究院文献>The Journal of Experimental Medicine >Exercise Provides Direct Biphasic Cardioprotection via Manganese Superoxide Dismutase Activation
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Exercise Provides Direct Biphasic Cardioprotection via Manganese Superoxide Dismutase Activation

机译：运动通过锰超氧化物歧化酶激活提供直接的双相心脏保护

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Epidemiologic investigations have shown that exercise reduces morbidity and mortality from coronary artery disease. In this study, using a rat model, we attempted to determine whether exercise can reduce ischemic injury to the heart and elucidate a mechanism for the cardioprotective effect of exercise. Results showed that exercise significantly reduced the magnitude of a myocardial infarction in biphasic manner. The time course for cardioprotection resembled that of the change in manganese superoxide dismutase (Mn-SOD) activity. The administration of the antisense oligodeoxyribonucleotide to Mn-SOD abolished the expected decrease in infarct size. We showed that the level of tumor necrosis factor α (TNF-α) and interleukin 1β (IL-1β) increased after exercise. The simultaneous administration of the neutralizing antibodies to the cytokines abolished the exercise-induced cardioprotection and the activation of Mn-SOD. Furthermore, TNF-α can mimic the biphasic pattern of cardioprotection and activation of Mn-SOD. An antioxidant completely abolished cardioprotection and the activation of Mn-SOD by exercise or the injection of TNF-α as well as exercise-induced increase in TNF-α and IL-1β. The production of reactive oxygen species and endogenous TNF-α and IL-1β induced by exercise leads to the activation of Mn-SOD, which plays major roles in the acquisition of biphasic cardioprotection against ischemia/reperfusion injury in rats.
机译：流行病学研究表明，运动可降低冠状动脉疾病的发病率和死亡率。在这项研究中，我们使用大鼠模型试图确定运动是否可以减轻心脏的缺血性损伤，并阐明运动对心脏的保护作用机制。结果表明，运动以双相方式显着降低了心肌梗塞的程度。心脏保护的时间过程类似于锰超氧化物歧化酶（Mn-SOD）活性的变化。对Mn-SOD施用反义寡脱氧核糖核苷酸消除了预期的梗塞面积减小。我们发现运动后肿瘤坏死因子α（TNF-α）和白介素1β（IL-1β）的水平升高。同时向细胞因子施用中和抗体消除了运动诱导的心脏保护和Mn-SOD的激活。此外，TNF-α可以模仿心脏保护和Mn-SOD激活的双相模式。抗氧化剂完全消除了通过运动或注射TNF-α以及运动引起的TNF-α和IL-1β的增加对心脏的保护和Mn-SOD的活化。运动引起的活性氧和内源性TNF-α和IL-1β的产生导致Mn-SOD的活化，这在获得大鼠抗缺血/再灌注双相心脏保护中起着重要作用。

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