Department of Biochemistry, Jawaharlal Nehru Medical College, Faculty of Medicine, Aligarh Muslim University, Aligarh 202002, Uttar Pradesh, India.
Department of Pharmacology, Jawaharlal Nehru Medical College, Faculty of Medicine, Aligarh Muslim University, Aligarh 202002, Uttar Pradesh, India.
Eur J Pharmacol. 2019 Apr 15;849:135-145. doi: 10.1016/j.ejphar.2019.01.056. Epub 2019 Feb 4.
Identification of pharmacologically potent antioxidant compounds for their use in preventive medicine is thrust area of current research. This study was undertaken with the aim of determining the protective role of syringic acid (SA) on isoproterenol (ISO) induced myocardial infarction (MI) in rats. SA was orally given to rats for 21 days at three different concentrations (12.5, 25 and 50 mg/kg). At 20th and 21st day, rats were subcutaneously injected with ISO and at the end of experimental period, rats were killed. ISO induced myocardial damage was averted by pre-co-treatment of SA, as decrease was found in serum level of marker enzymes (CKMB, LDH, AST, ALT), lipid peroxidation, protein carbonyl (PC) and proinflammatory cytokines (TNFα, IL 6). Furthermore, content of glutathione (GSH) and activities of antioxidant enzymes in heart tissue were significantly raised. Improvement in infarct size and erythrocyte (RBCs) morphology was also observed. The biochemical findings were supported by histopathological outcome and protective effect of SA was found to be dose dependent. The results of our study demonstrated that the cardioprotective potential of SA in rat model of ISO induced MI might be due to anti-lipid peroxidative and endogenous antioxidant system enhancement effects.
鉴定具有药理活性的抗氧化化合物并将其用于预防医学是当前研究的热点领域。本研究旨在确定丁香酸（SA）对异丙肾上腺素（ISO）诱导的大鼠心肌梗死（MI）的保护作用。SA 以三种不同浓度（12.5、25 和 50mg/kg）经口给予大鼠 21 天。在第 20 天和第 21 天，大鼠皮下注射 ISO，在实验期末处死大鼠。SA 的预先治疗可避免 ISO 诱导的心肌损伤，因为标记酶（CKMB、LDH、AST、ALT）、脂质过氧化、蛋白羰基（PC）和促炎细胞因子（TNFα、IL-6）的血清水平降低。此外，心脏组织中的谷胱甘肽（GSH）含量和抗氧化酶活性显著升高。梗死面积和红细胞（RBC）形态的改善也观察到。生化发现得到了组织病理学结果的支持，并且发现 SA 的保护作用呈剂量依赖性。我们的研究结果表明，SA 在 ISO 诱导的 MI 大鼠模型中的心脏保护作用可能归因于抗脂质过氧化和增强内源性抗氧化系统的作用。
