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Protective Role of Oxycodone in Myocardial Oxidative Stress and Mitochondrial Dysfunction Induced by Ischemia-Reperfusion

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机构: [1]Peoples Hosp Jiawang Dist Xuzhou City, Xuzhou, Peoples R China [2]Hebei Univ, Affiliated Hosp, Dept Cardiol, Baoding, Peoples R China
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关键词: membrane potential mitochondria oxidative stress reperfusion injury signal transduction

摘要:
Ischemia-reperfusion (I/R) injury is a significant clinical problem impacting the heart and other organs, such as the kidneys and liver. This study explores the protective effects of oxycodone on myocardial I/R injury and its underlying mechanisms. Using a myocardial I/R model in Sprague-Dawley (SD) rats and an oxygen-glucose deprivation/reoxygenation (OGD/R) model in H9c2 cells, we administered oxycodone and inhibited AMP-activated protein kinase (AMPK) with Compound C (C.C). Our results showed that oxycodone significantly reduced lactate dehydrogenase (LDH) release and reactive oxygen species (ROS) production while stabilizing mitochondrial membrane potential (MMP). Western blot and RT-qPCR analyzes confirmed that oxycodone enhances AMPK phosphorylation and upregulates the expression of Silent Information Regulator 1 (SIRT1) and Peroxisome Proliferator-Activated Receptor gamma Coactivator 1 alpha (PGC-1 alpha), thereby protecting myocardial cells. These findings suggest that oxycodone exerts significant protective effects against I/R injury by activating the AMPK pathway, offering new potential therapeutic targets for myocardial protection.

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大类 | 3 区 医学
小类 | 3 区 生化与分子生物学 3 区 毒理学
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最新[2023]版:
Q2 BIOCHEMISTRY & MOLECULAR BIOLOGY Q2 TOXICOLOGY

影响因子: 最新[2023版] 最新五年平均 出版当年[2025版] 出版当年五年平均 出版前一年[2024版]

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第一作者机构: [1]Peoples Hosp Jiawang Dist Xuzhou City, Xuzhou, Peoples R China
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