Department of Pharmacology and Toxicology, College of Pharmacy, King Saud University, Riyadh, Saudi Arabia.
Department of Pharmacology College of Pharmacy, Princess Nora Bint Abdul Rahman University, Riyadh, Saudi Arabia.
J Cell Biochem. 2018 May;119(5):3903-3912. doi: 10.1002/jcb.26530. Epub 2018 Jan 23.
Several studies have reported that metformin is cardioprotective for diabetic and non-diabetic ischemic hearts through mechanisms that cannot be entirely attributed to its anti-hyperglycemic effect. This study was designed to investigate the cardioprotective effects of metformin with and without vitamin E after induction myocardial infarction (MI) in rats, using isoproterenol. Administration of metformin or vitamin E significantly reduced the cardiac mass index (P < 0.01), ameliorated the changes to cardiac biomarkers, and attenuated oxidative stress levels compared to the isoproterenol group. Interestingly, combination therapy showed a slight synergistic effect. Histopathological analysis suggested that metformin treatment reduced NF-κB expression and protected against isoproterenol-induced MI. Our results indicate that metformin mediates a cardioprotective effect against isoproterenol-induced MI via antioxidant activity and modulation of the NF-κB signaling pathway. This suggests that metformin would be beneficial in MI treatment.
几项研究报告称,二甲双胍通过不能完全归因于其降血糖作用的机制对糖尿病和非糖尿病缺血性心脏具有心脏保护作用。本研究旨在使用异丙肾上腺素诱导大鼠心肌梗死后,研究二甲双胍联合和不联合维生素 E 的心脏保护作用。与异丙肾上腺素组相比,二甲双胍或维生素 E 的给药显著降低了心脏质量指数(P < 0.01),改善了心脏生物标志物的变化,并减轻了氧化应激水平。有趣的是,联合治疗显示出轻微的协同作用。组织病理学分析表明,二甲双胍治疗可降低 NF-κB 表达并防止异丙肾上腺素诱导的 MI。我们的结果表明,二甲双胍通过抗氧化活性和调节 NF-κB 信号通路对异丙肾上腺素诱导的 MI 发挥心脏保护作用。这表明二甲双胍在 MI 治疗中可能有益。