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Diazoxide-induced cardioprotection via Delta Psi m loss depending on timing of application

机译：二氧嗪诱导的Delta Psi m损失引起的心脏保护作用取决于应用时间

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Although the role of mitochondrial ATP-sensitive potassium (mitoK(ATP)) channels in cardioprotection is widely accepted, it remains unclear when their opening is critical for protection. We tested the hypothesis that the mitoK(ATP) channel acts as a trigger or mediator of protection against apoptosis through loss of mitochondrial inner membrane potential (Delta Psi m). Exposure of neonatal rat cardiomyocytes to H2O2 (0.5 mmol/L) resulted in apoptosis associated with severe Delta Psi m loss. Pretreatment with diazoxide (20 to 100 mu mol/L) prevented H2O2-induced apoptosis and Delta Psi m loss at 2 but not 18 h after exposure, while the latter was prevented by cotreatment with diazoxide. Lack of protection by pretreatment with diazoxide was observed in cardiomyocytes cultured in a medium containing H2O2 for 2 h and then not containing for 16 h. The slopes of the regression lines of the relationship between the proportion of apoptotic cells and Delta Psi m loss (y=-0.89 vs. -0.42) and the proportion of cells with high side scatter signal differed between cardiomyocytes exposed H2O2 for 2 and 18 It. Diazoxide per se caused a transient Delta Psi m loss (within 30 min) with a recovery followed by persistent Delta Psi m loss (after 6 h). Inhibition of the former by 5-hydroxydecanoate (5-HD, 0.5 mmol/L) abolished protection of pretreatment with diazoxide (trigger phase), while that of the latter prevented the protection of cotreatment with diazoxide (mediator phase). Our results suggest that mitoK(ATP) channels act as a trigger and mediator of cardioprotection through a transient or persistent Delta Psi m loss depending on phenotypic consequence in response to oxidants. (c) 2006 Elsevier Inc. All rights reserved.
机译：虽然线粒体ATP敏感性钾（mitoK（ATP））通道在心脏保护中的作用已被广泛接受，但尚不清楚何时开放对保护至关重要。我们测试了以下假设，即mitoK（ATP）通道可通过线粒体内膜电位（Delta Psi m）的丧失来防止细胞凋亡。新生大鼠心肌细胞暴露于H2O2（0.5 mmol / L）会导致细胞凋亡，并伴有严重的Delta Psi m丢失。用二氮嗪（20至100μmol/ L）预处理可防止H2O2诱导的细胞凋亡和Delta Psi m损失，但在暴露后2 h而非18 h即可，而后者可通过与diazoxide共同处理来预防。在含有H2O2的培养基中培养了2h，然后不含H2O2的培养基中培养的心肌细胞中，未观察到用二氮嗪进行预处理时缺乏保护作用。在暴露于H2O2 2和18的心肌细胞之间，凋亡细胞比例与Delta Psi m损失之间的关系（y = -0.89 vs.-0.42）与具有高侧向散射信号的细胞比例之间的回归线的斜率不同。 。二氮嗪本身导致短暂的Delta Psi m损失（在30分钟内）并恢复，随后持续的Delta Psi m损失（6小时后）。 5-羟基癸酸酯（5-HD，0.5 mmol / L）对前者的抑制作用取消了对重氮氧化物（触发相）预处理的保护，而对后者的保护则阻止了对重氮氧化物（介导相）的预处理的保护。我们的结果表明，mitoK（ATP）通道通过短暂或持续的Delta Psi m丢失，根据对氧化剂的反应的表型结果，作为心脏保护的触发剂和介质。 （c）2006 Elsevier Inc.保留所有权利。

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