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N-acetylcysteine Treatment Prevents the Up-Regulation of MnSOD in Chronically Hypoxic Rat Hearts

机译:N-乙酰半胱氨酸治疗可预防慢性缺氧大鼠心脏中MnSOD的上调

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摘要

Chronic intermittent hypoxia (CIH) is associated with increased production of reactive oxygen species that contributes to the adaptive mechanism underlying the improved myocardial ischemic tolerance. The aim was to find out whether the antioxidative enzyme manganese superoxide dismutase (MnSOD) can play a role in CIH-induced cardioprotection. Adult male Wistar rats were exposed to intermittent hypobaric hypoxia (7000 m, 8 h/day, 25 exposures) (n=14) or kept at normoxia (n=14). Half of the animals from each group received N-acetylcysteine (NAC, 100 mg/kg) daily before the hypoxic exposure. The activity and expression of MnSOD were increased by 66 % and 23 %, respectively, in the mitochondrial fraction of CIH hearts as compared with the normoxic group; these effects were suppressed by NAC treatment. The negative correlation between MnSOD activity and myocardial infarct size suggests that MnSOD can contribute to the improved ischemic tolerance of CIH hearts.
机译:慢性间歇性缺氧(CIH)与活性氧的产生增加有关,这有助于改善心肌缺血耐受性的适应机制。目的是发现抗氧化酶锰超氧化物歧化酶(MnSOD)是否可以在CIH诱导的心脏保护中发挥作用。成年雄性Wistar大鼠暴露于间歇性低压缺氧(7000 m,8 h / day,25次暴露)(n = 14)或保持常氧(n = 14)。每组一半的动物每天在低氧暴露前接受N-乙酰半胱氨酸(NAC,100 mg / kg)。与常氧组相比,CIH心脏线粒体中MnSOD的活性和表达分别增加了66%和23%。这些作用被NAC治疗所抑制。 MnSOD活性与心肌梗死面积之间呈负相关关系,表明MnSOD可以改善CIH心脏的缺血耐受性。

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