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<p>Myocardial infarction (MI) remains a major cause of morbidity and mortality worldwide, primarily driven by oxidative stress, inflammation, and apoptosis. The present study investigated the cardioprotective potential of opuntiol using both in vitro and in vivo approaches. In vitro, cardiomyocytes were treated with isoproterenol (ISO) to induce cytotoxicity, and the effects of opuntiol was evaluated using MTT assay for cell viability, ROS generation assessment, and apoptosis dual staining. Opuntiol significantly enhanced cell viability, reduced intracellular ROS, and decreased apoptotic cell populations in a dose-dependent manner. In vivo, the cardioprotective potential of opuntiol against ISO-induced MI was evaluated in Wistar rats. The male rats were divided into four groups: Group I: Control, Group II: Opuntiol alone (100&#xa0;mg/kg), Group III: ISO alone (85&#xa0;mg/kg, s.c., on days 13 and 14), Group IV: Opuntiol + ISO treatment, and then opuntiol administration orally for 14&#xa0;days before ISO administration. Biochemical markers of cardiac injury (cTn-T, cTn-I, CK, CK-MB, LDH), oxidative stress (TBARS, LOOH, SOD, CAT, GPx, GSH), inflammatory cytokines (TNF-α, IL-6, NF-κB), and apoptotic gene expression (Bax, Bcl-2, Caspase-3, -9, Cytochrome c) were assessed. ISO treatment significantly elevated cardiac biomarkers, lipid peroxidation, and pro-inflammatory cytokines, while reducing antioxidant enzyme levels and triggering the expression of pro-apoptotic proteins/genes. Opuntiol pre-treatment conferred dose-dependent protection by normalizing cardiac enzyme levels, suppressing lipid peroxidation, enhancing antioxidant status, and downregulating pro-inflammatory and apoptotic markers. Notably, the highest dose (100&#xa0;mg/kg) of opuntiol restored biochemical and molecular parameters close to those of the control group. These findings suggest that opuntiol exerts potent cardioprotective effects through its antioxidant, anti-inflammatory, and anti-apoptotic mechanisms. The modulation of TNF-α, IL-6, NF-κB, and mitochondrial apoptosis-related genes underscores the therapeutic potential of this approach in cardiac injury. This study highlights the importance of opuntiol as a promising natural compound for the prevention and management of myocardial infarction.</p>

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Cardioprotective effect of opuntiol on isoproterenol-induced myocardial infarction in male albino Wistar rats

  • 期刊论文

  • 发表日期：

    2026年7月28日

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  • Na Wang,
  • Hao Wang,
  • Fan Zhang,
  • Hongxin Zhu,
  • Zheng Ren,
  • Luyao Zheng

摘要

Myocardial infarction (MI) remains a major cause of morbidity and mortality worldwide, primarily driven by oxidative stress, inflammation, and apoptosis. The present study investigated the cardioprotective potential of opuntiol using both in vitro and in vivo approaches. In vitro, cardiomyocytes were treated with isoproterenol (ISO) to induce cytotoxicity, and the effects of opuntiol was evaluated using MTT assay for cell viability, ROS generation assessment, and apoptosis dual staining. Opuntiol significantly enhanced cell viability, reduced intracellular ROS, and decreased apoptotic cell populations in a dose-dependent manner. In vivo, the cardioprotective potential of opuntiol against ISO-induced MI was evaluated in Wistar rats. The male rats were divided into four groups: Group I: Control, Group II: Opuntiol alone (100 mg/kg), Group III: ISO alone (85 mg/kg, s.c., on days 13 and 14), Group IV: Opuntiol + ISO treatment, and then opuntiol administration orally for 14 days before ISO administration. Biochemical markers of cardiac injury (cTn-T, cTn-I, CK, CK-MB, LDH), oxidative stress (TBARS, LOOH, SOD, CAT, GPx, GSH), inflammatory cytokines (TNF-α, IL-6, NF-κB), and apoptotic gene expression (Bax, Bcl-2, Caspase-3, -9, Cytochrome c) were assessed. ISO treatment significantly elevated cardiac biomarkers, lipid peroxidation, and pro-inflammatory cytokines, while reducing antioxidant enzyme levels and triggering the expression of pro-apoptotic proteins/genes. Opuntiol pre-treatment conferred dose-dependent protection by normalizing cardiac enzyme levels, suppressing lipid peroxidation, enhancing antioxidant status, and downregulating pro-inflammatory and apoptotic markers. Notably, the highest dose (100 mg/kg) of opuntiol restored biochemical and molecular parameters close to those of the control group. These findings suggest that opuntiol exerts potent cardioprotective effects through its antioxidant, anti-inflammatory, and anti-apoptotic mechanisms. The modulation of TNF-α, IL-6, NF-κB, and mitochondrial apoptosis-related genes underscores the therapeutic potential of this approach in cardiac injury. This study highlights the importance of opuntiol as a promising natural compound for the prevention and management of myocardial infarction.