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

IF 2.8 3区医学 Q2 BIOCHEMISTRY & MOLECULAR BIOLOGY Journal of Biochemical and Molecular Toxicology Pub Date : 2025-01-26 DOI:10.1002/jbt.70151

Yongzheng Jiang, Hua He, Xinwei Jia

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Abstract

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 γ Coactivator 1α (PGC-1α), 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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羟考酮对缺血再灌注心肌氧化应激和线粒体功能障碍的保护作用。

缺血再灌注（I/R）损伤是影响心脏和其他器官（如肾脏和肝脏）的重要临床问题。本研究探讨氧可酮对心肌I/R损伤的保护作用及其机制。采用Sprague-Dawley （SD）大鼠心肌I/R模型和H9c2细胞氧-葡萄糖剥夺/再氧化（OGD/R）模型，我们给药羟考酮和化合物C （C.C）抑制amp活化蛋白激酶（AMPK）。我们的研究结果表明，氧可酮显著降低乳酸脱氢酶（LDH）的释放和活性氧（ROS）的产生，同时稳定线粒体膜电位（MMP）。Western blot和RT-qPCR分析证实，羟考酮可增强AMPK磷酸化，上调沉默信息调节因子1 （SIRT1）和过氧化物酶体增殖物激活受体γ共激活因子1α (PGC-1α)的表达，从而保护心肌细胞。这些发现表明，羟考酮通过激活AMPK通路对I/R损伤具有显著的保护作用，为心肌保护提供了新的潜在治疗靶点。

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索莱宝

oxycodone

来源期刊

Journal of Biochemical and Molecular Toxicology 生物-毒理学

CiteScore

5.80

自引率

2.80%

发文量

277

审稿时长

6-12 weeks

期刊介绍： The Journal of Biochemical and Molecular Toxicology is an international journal that contains original research papers, rapid communications, mini-reviews, and book reviews, all focusing on the molecular mechanisms of action and detoxication of exogenous and endogenous chemicals and toxic agents. The scope includes effects on the organism at all stages of development, on organ systems, tissues, and cells as well as on enzymes, receptors, hormones, and genes. The biochemical and molecular aspects of uptake, transport, storage, excretion, lactivation and detoxication of drugs, agricultural, industrial and environmental chemicals, natural products and food additives are all subjects suitable for publication. Of particular interest are aspects of molecular biology related to biochemical toxicology. These include studies of the expression of genes related to detoxication and activation enzymes, toxicants with modes of action involving effects on nucleic acids, gene expression and protein synthesis, and the toxicity of products derived from biotechnology.