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首页> 美国卫生研究院文献>Oxidative Medicine and Cellular Longevity >N-n-Butyl Haloperidol Iodide Ameliorates Cardiomyocytes Hypoxia/Reoxygenation Injury by Extracellular Calcium-Dependent and -Independent Mechanisms
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N-n-Butyl Haloperidol Iodide Ameliorates Cardiomyocytes Hypoxia/Reoxygenation Injury by Extracellular Calcium-Dependent and -Independent Mechanisms

机译：N-正丁基氟哌啶醇碘化物通过细胞外钙依赖性和非依赖性机制改善心肌细胞的缺氧/复氧损伤

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N-n-butyl haloperidol iodide (F2) has been shown to antagonize myocardial ischemia/reperfusion injury by blocking calcium channels. This study explores the biological functions of ERK pathway in cardiomyocytes hypoxia/reoxygenation injury and clarifies the mechanisms by which F2 ameliorates cardiomyocytes hypoxia/reoxygenation injury through the extracellular-calcium-dependent and -independent ERK1/2-related pathways. In extracellularcalcium-containing hypoxia/reoxygenation cardiomyocytes, PKCα and ERK1/2 were activated, Egr-1 protein level and cTnI leakage increased, and cell viability decreased. The ERK1/2 inhibitors suppressed extracellular-calcium-containing-hypoxia/reoxygenation-induced Egr-1 overexpression and cardiomyocytes injury. PKCα inhibitor downregulated extracellularcalcium-containing-hypoxia/reoxygenation-induced increase in p-ERK1/2 and Egr-1 expression. F2 downregulated hypoxia/reoxygenation-induced elevation of p-PKCα, p-ERK1/2, and Egr-1 expression and inhibited cardiomyocytes damage. The ERK1/2 and PKCα activators antagonized F2's effects. In extracellular-calcium-free-hypoxia/reoxygenation cardiomyocytes, ERK1/2 was activated, LDH and cTnI leakage increased, and cell viability decreased. F2 and ERK1/2 inhibitors antagonized extracellular-calcium-free-hypoxia/reoxygenation-induced ERK1/2 activation and suppressed cardiomyocytes damage. The ERK1/2 activator antagonized F2's above effects. F2 had no effect on cardiomyocyte cAMP content or PKA and Egr-1 expression. Altogether, ERK activation in extracellular-calcium-containing and extracellular-calcium-free hypoxia/reoxygenation leads to cardiomyocytes damage. F2 may ameliorate cardiomyocytes hypoxia/reoxygenation injury by regulating the extracellular-calcium-dependent PKCα/ERK1/2/Egr-1 pathway and through the extracellular-calcium-independent ERK1/2 activation independently of the cAMP/PKA pathway or Egr-1 overexpression.
机译：N-正丁基氟哌啶醇碘化物（F2）已显示可通过阻断钙通道来拮抗心肌缺血/再灌注损伤。这项研究探讨了ERK通路在心肌细胞缺氧/复氧损伤中的生物学功能，并阐明了F2通过细胞外钙依赖性和独立于ERK1 / 2相关途径改善心肌细胞缺氧/复氧损伤的机制。在细胞外含钙的缺氧/复氧心肌细胞中，PKCα和ERK1 / 2被激活，Egr-1蛋白水平和cTnI渗漏增加，细胞活力降低。 ERK1 / 2抑制剂抑制细胞外含钙的缺氧/复氧诱导的Egr-1过表达和心肌细胞损伤。 PKCα抑制剂下调细胞外含钙的缺氧/复氧诱导的p-ERK1 / 2和Egr-1表达的增加。 F2下调了缺氧/复氧诱导的p-PKCα，p-ERK1 / 2和Egr-1表达的升高，并抑制了心肌细胞的损伤。 ERK1 / 2和PKCα激活剂拮抗F2的作用。在细胞外无钙缺氧/复氧心肌细胞中，ERK1 / 2被激活，LDH和cTnI泄漏增加，细胞活力降低。 F2和ERK1 / 2抑制剂拮抗细胞外无钙缺氧/复氧诱导的ERK1 / 2活化并抑制心肌细胞的损害。 ERK1 / 2激活剂拮抗F2的上述作用。 F2对心肌细胞cAMP含量或PKA和Egr-1表达没有影响。总之，含细胞外钙和无细胞外钙的缺氧/复氧中的ERK活化会导致心肌细胞损伤。 F2可以通过调节细胞外钙依赖性的PKCα/ ERK1 / 2 / Egr-1途径并通过独立于cAMP / PKA途径或Egr-1过表达的细胞外钙依赖性的ERK1 / 2活化来减轻心肌的缺氧/复氧损伤。

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