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首页> 外文期刊>Canadian Journal of Physiology and Pharmacology >Role of oxidative stress in ischemia-reperfusion-induced alterations in myofibrillar ATPase activities and gene expression in the heart.
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Role of oxidative stress in ischemia-reperfusion-induced alterations in myofibrillar ATPase activities and gene expression in the heart.

机译：氧化应激在缺血再灌注诱导的肌原纤维ATPase活性和心脏基因表达中的作用。

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Ischemia-reperfusion (IR) in the heart has been shown to produce myofibrillar remodeling and depress Ca2+ sensitivity of myofilaments; however, the mechanisms for these alterations are not clearly understood. In view of the role of oxidative stress in cardiac dysfunction due to IR, isolated rat hearts were subjected to global ischemia for 30 min followed by a 30-minute period of reperfusion. IR was found to induce cardiac dysfunction, as reflected by depressed LVDP, +dP/dt, and -dP/dt, and elevated LVEDP, and to reduce myofibrillar Ca2+-stimulated ATPase activity. These changes were simulated by perfusing the hearts with a mixture of xanthine plus xanthine oxidase, which is known to generate oxyradicals. The alterations in cardiac function and myofibrillar Ca2+-stimulated ATPase in IR hearts were attenuated by pretreatment with antioxidants (superoxide dismutase plus catalase, and N-acetylcysteine) and leupeptin, an inhibitor of Ca2+-dependent protease. The levels of mRNA for myosin heavy chain isoforms (alpha-MHC and beta-MHC) and myosin light chain (MLC1) were depressed in IR hearts. These changes in gene expression due to IR were prevented upon perfusing the hearts with superoxide plus catalase, with N-acetylcysteine, or with leupeptin. The results suggest that oxidative stress due to IR injury and associated proteolysis play an important role in inducing changes in myofibrillar Ca2+-stimulated ATPase activity and gene expression in the heart.
机译：心脏中的缺血再灌注（IR）已显示可引起肌原纤维重塑，并降低肌丝的Ca2 +敏感性。但是，这些更改的机制尚不清楚。考虑到氧化应激在由IR引起的心脏功能障碍中的作用，对离体大鼠心脏进行了30分钟的整体缺血，然后再进行30分钟的再灌注。发现IR可诱发心脏功能障碍，如LVDP降低，+ dP / dt和-dP / dt以及LVEDP升高所反映，并降低肌原纤维Ca2 +刺激的ATPase活性。通过用黄嘌呤加黄嘌呤氧化酶的混合物灌注心脏来模拟这些变化，已知黄嘌呤加黄嘌呤氧化酶会产生羟自由基。通过抗氧化剂（超氧化物歧化酶加过氧化氢酶和N-乙酰半胱氨酸）和亮肽素（一种依赖Ca2 +的蛋白酶的抑制剂）进行预处理，可以减轻IR心脏的心脏功能和肌原纤维Ca2 +刺激的ATPase的变化。 IR心脏中的肌球蛋白重链亚型（α-MHC和β-MHC）和肌球蛋白轻链（MLC1）的mRNA水平降低。当用超氧化物加过氧化氢酶，N-乙酰半胱氨酸或亮肽素灌注心脏时，可防止由于IR引起的基因表达的这些变化。结果表明，由IR损伤引起的氧化应激和相关的蛋白水解在诱导肌原纤维Ca2 +刺激的ATPase活性和心脏基因表达的变化中起重要作用。

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