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Cardioprotective Effect of 'Methylamine Irisolidone', a New Compound, in Hypoxia/Reoxygenation Injury in Cultured Rat Cardiac Myocytes

机译:新化合物“甲胺基固酮”对大鼠心肌细胞缺氧/复氧损伤的保护作用

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摘要

'Methylamine irisolidone' (=5,7-dihydroxy-6-methoxy-3-(4-methoxyphenyl)-8-[(methylamino)-methyl]-4 H-[1]benzopyran-4-one), a new compound, is a structurally modified kakkalide with good water solubility. In this study, we investigated its effect on hypoxia/reoxygenation (H/R) injury in cultured rat cardiac myocytes. ne results showed that methylamine irisolidone could significantly inhibit lactate dehydrogenase (LDH) release, enhance the mitochondrial membrane potential, decrease intracellular calcium (Ca2+) associated with the attenuation of reactive oxygen species (ROS) generation, reduce contents of malondialdehyde (MDA), and increase the activity of superoxide dismutase (SOD) after H/R in a dose-dependent manner. The present study demonstrated that methylamine irisolidone can directly protect cardiomyocytes against H/R injury, primarily as a result of reduction of the intracellular Ca2+ overload coincident with an attenuation of ROS generation and ROS-mediated lipid peroxidation, which may contribute to the preservation of mitochondrion function and antioxidant against H/R injury.
机译:一种新化合物“甲胺irisolidone”(= 5,7-二羟基-6-甲氧基-3-(4-甲氧基苯基)-8-[(甲氨基)-甲基] -4 H- [1]苯并吡喃-4-酮) ,是一种具有良好水溶性的结构改性kakkalide。在这项研究中,我们调查了其对培养的大鼠心肌细胞缺氧/复氧(H / R)损伤的影响。结果表明,甲胺西立酮可以显着抑制乳酸脱氢酶(LDH)的释放,增强线粒体膜电位,降低细胞内钙(Ca2 +),从而降低活性氧(ROS)的产生,降低丙二醛(MDA)的含量,以及在H / R后以剂量依赖性方式增加超氧化物歧化酶(SOD)的活性。本研究表明甲胺西立酮可以直接保护心肌细胞免受H / R损伤,这主要是由于细胞内Ca2 +超载的减少与ROS生成的减弱和ROS介导的脂质过氧化作用的结合,这可能有助于线粒体的保存功能和抗H / R损伤的抗氧化剂。

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