Cardioprotective Effect of Nano Gold Kalimag Injection via Inhibiting Oxidative Stress and Improving Myocardial Energy Metabolism in Ischemic Heart Injury Model

Jin-A Cha, Un-Rim Sim, Song-Chol Mun, Ji-Myong Kim, Kwon-Gi Kang, Sol-Hyang Choe
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Abstract

Many people worldwide die from cardiovascular diseases. Myocardial ischemia can be induced by atherosclerosis, and the main factor responsible for atherosclerosis is the deposition of lipid peroxide in vessels. Therefore, atherogenesis may be prevented and treated at the cellular level by preventing oxidative stress using the properties of nanogold, magnesium and potassium. In this study, we have elucidated the cardioprotective effect of Nano Gold Kalimag injection (NGKM) in the ischemic heart injury model in rats. The ischemic heart injury models were made with adrenaline and pituitrin, and a few myocardial damage-related parameters of the models were observed after NGKM injection. After NGKM injection, the levels of lactate dehydrogenase (LDH), aspartate transamiase (AST), and creatine kinase (CK) in an ischemic heart injury model in rats were detected, and TTC staining and H&E staining were performed. In addition, in the myocardial tissues of rats, superoxide dismutase (SOD), malondialdehyde (MDA), glutathione peroxidase (GSH-Px), catalase, and Na+-K+-ATPase activity were measured, and lactate content and ATP content were measured. NGKM can reduce the infarct area in the ischemic heart injury model and significantly lower LDH, AST, and CK levels. SOD, GSH-Px, and arterial tissue CAT levels significantly increased compared to the model, and MDA contents significantly decreased in myocardial tissue compared to the model group. In addition, myocardial tissue ATP content and Na+-K+-ATPase level in myocardial tissues significantly increased compared to the model group, and lactate content in myocardial tissue significantly decreased compared to the model group. Our findings suggest that NGKM injection has cardioprotective effects by inhibiting oxidative stress in an ischemic heart injury model in rats.
纳米金卡利马格注射液通过抑制氧化应激和改善缺血性心脏损伤模型心肌能量代谢对心脏的保护作用
全世界有许多人死于心血管疾病。动脉粥样硬化可诱发心肌缺血,而造成动脉粥样硬化的主要因素是过氧化脂质在血管中的沉积。因此,可以利用纳米金、镁和钾的特性防止氧化应激,从而在细胞水平上预防和治疗动脉粥样硬化。本研究阐明了纳米金卡利马格注射液(NGKM)在大鼠缺血性心脏损伤模型中的心脏保护作用。用肾上腺素和垂体促肾上腺素制作缺血性心脏损伤模型,注射 NGKM 后观察了模型的一些心肌损伤相关参数。注射 NGKM 后,检测了缺血性心脏损伤模型大鼠的乳酸脱氢酶(LDH)、天冬氨酸转氨酶(AST)和肌酸激酶(CK)水平,并进行了 TTC 染色和 H&E 染色。此外,还测定了大鼠心肌组织中的超氧化物歧化酶(SOD)、丙二醛(MDA)、谷胱甘肽过氧化物酶(GSH-Px)、过氧化氢酶和 Na+-K+-ATP 酶的活性,以及乳酸含量和 ATP 含量。NGKM能缩小缺血性心脏损伤模型的梗死面积,并显著降低LDH、AST和CK水平。与模型组相比,心肌组织中的 SOD、GSH-Px 和动脉组织 CAT 含量明显升高,MDA 含量明显降低。此外,与模型组相比,心肌组织中的 ATP 含量和 Na+-K+-ATP 酶水平明显升高,心肌组织中的乳酸含量明显降低。我们的研究结果表明,在大鼠缺血性心脏损伤模型中,注射 NGKM 可抑制氧化应激,从而起到保护心脏的作用。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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