Late ischemic preconditioning is mediated in myocytes by enhanced endogenous antioxidant activity stimulated by oxygen-derived free radicals.
Late ischemic preconditioning is mediated in myocytes by enhanced endogenous antioxidant activity stimulated by oxygen-derived free radicals.
复制标题
肌细胞中的晚期缺血预处理是通过氧自由基刺激的内源性抗氧化活性增强来介导的。
DOI：
10.1111/j.1749-6632.1996.tb33512.x
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发表时间：
1996
影响因子：
5.2
通讯作者：
Ashraf,M
中科院分区：
文献类型：
--
作者：
Zhai,X;Zhou,X;Ashraf,M
该研究的主要目的是检验以下假设：初始缺氧期间氧自由基会刺激肌细胞后期预处理中的内源性抗氧化活性。一组用5分钟缺氧和5分钟复氧的两个循环对分离的大鼠肌细胞进行预处理，另一组用黄嘌呤氧化酶与黄嘌呤反应产生的外源超氧阴离子(.O2-)进行预处理。肌细胞保存24小时，然后暴露于60分钟缺氧和60分钟复氧。预处理的心肌细胞表现出LDH释放减少、丙二醛形成减少、细胞活力增加和细胞结构保存完好。重复缺氧（1.65+/-0.08 nmol/mg蛋白质）或外源性处理后，心肌细胞的O2产生立即增加。 O2-（1.42+/-0.11 nmol/mg 蛋白质）。别嘌呤醇，一种黄嘌呤氧化酶抑制剂，被废除。初始预处理期间产生氧气。 24 小时后，缺氧对照肌细胞中 Mn SOD 活性下降（0.38+/-0.06 U/mg 蛋白），而在重复缺氧（3.25+/-0.15 nmol/mg 蛋白）或外源性预处理的肌细胞中，Mn SOD 活性显着增加。 O2-（2.27+/-0.10 nmol/mg 蛋白质）。在预处理的心肌细胞中观察到的 Mn SOD 活性增加和心肌保护作用被别嘌呤醇完全阻断。这些结果表明，初始预处理期间产生的氧自由基在24小时后激活内源性抗氧化防御（Mn SOD活性增加），这有助于预处理的后期心脏保护。
The primary objective of the study was to test the hypothesis that oxygen radical during initial anoxia stimulate endogenous antioxidant activity in late preconditioning in myocytes. Isolated rat myocytes were preconditioned in one group with two cycles of 5 minutes of anoxia and 5 minutes of reoxygenation and in another group with exogenous superoxide anion (. O2-) generated by reaction of xanthine oxidase with xanthine. Myocytes were kept for 24 hours, after which they were exposed to 60 minutes of anoxia and 60 minutes of reoxygenation. Preconditioned myocytes exhibited decreased LDH release, reduced malondialdehyde formation, increased cell viability, and well-preserved cell structure.. O2-production was increased in myocytes immediately after treatment with repetitive anoxia (1.65+/-0.08 nmol/mg protein) or exogenous. O2-(1.42+/-0.11 nmol/mg protein). Allopurinol, a xanthine oxidase inhibitor, abolished. O2-production during the initial preconditioning period. Twenty-four hours later, Mn SOD activity declined in anoxic control myocytes (0.38+/-0.06 U/mg protein), whereas it increased significantly in myocytes preconditioned with repetitive anoxia (3.25+/-0.15 nmol/mg protein) or with exogenous. O2-(2.27+/-0.10 nmol/mg protein). The increase in Mn SOD activity and myocardial protective effects observed in preconditioned myocytes were totally blocked by allopurinol. These results indicate that oxygen radicals generated during the initial preconditioning period activate endogenous antioxidant defense (increased Mn SOD activity) 24 hours later, which contributes to the late cardioprotection of preconditioning.