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Protective effect of morin on cardiac mitochondrial function during isoproterenol-induced myocardial infarction in male Wistar rats

机译:茉莉酸对异丙肾上腺素诱发的雄性Wistar大鼠心肌梗死后心脏线粒体功能的保护作用

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Altered mitochondrial function and free radical-mediated tissue damage have been suggested as an important pathological event in isoproterenol (ISO)-induced cardiotoxicity. This study was undertaken to know the preventive effect of morin on mitochondrial damage in ISO-induced cardiotoxicity in male Wistar rats. Myocardial infarction (MI) in rats was induced by ISO (85 mg/kg) at an interval of 24 hours for 2 days. Morin was given to rats as pre-treatment for 30 days orally using an intragastric tube. ISO-treated rats showed a significant elevation of mitochondrial thiobarbituric acid reactive substances (TBARS) and hydrogen peroxide (HP) level and pre-treatment with morin significantly prevented the increase of TBARS and HP level to near normality. The level of enzymic and non-enzymic antioxidants was decreased significantly in ISO-treated rats and pre-treatment with morin significantly increased the levels of superoxide dismutase, catalase, glutathione peroxidase, glutathione-S-transferase, glutathione reductase, and reduced glutathione to normality. The activities of mitochondrial enzymes such as isocitrate dehydrogenase, alpha-ketoglutarate dehydrogenase, succinate dehydrogenase, and malate dehydrogenase were decreased significantly in ISO-treated myocardial ischemic rats and upon pre-treatment with morin restored these enzymes activity to normality. In addition, the decreased activities of cytochrome-C oxidase and NADH-dehydrogenases were observed in ISO-treated rats and pre-treatment with morin prevented the activities of cytochrome-C oxidase and NADH-dehydrogenase to normality. Pre-treatment with morin favorably restored the biochemical and functional parameters to near normal indicating morin to be a significant protective effect on cardiac mitochondrial function against ISO-induced MI in rats.
机译:线粒体功能的改变和自由基介导的组织损伤已被认为是异丙肾上腺素(ISO)诱导的心脏毒性的重要病理事件。进行这项研究是为了了解茉莉香粉对ISO诱导的雄性Wistar大鼠心脏毒性中线粒体损伤的预防作用。 ISO(85 mg / kg)每隔24小时诱导大鼠心肌梗死(MI),持续2天。使用胃内导管口服向大鼠喂以吗啉以进行30天的预处理。用ISO治疗的大鼠显示线粒体硫代巴比妥酸反应性物质(TBARS)和过氧化氢(HP)含量显着升高,而用morin预处理可显着阻止TBARS和HP含量升高至接近正常水平。在用ISO治疗的大鼠中,酶促和非酶促抗氧化剂的水平显着降低,而用morin预处理则显着增加了超氧化物歧化酶,过氧化氢酶,谷胱甘肽过氧化物酶,谷胱甘肽S-转移酶,谷胱甘肽还原酶的水平,并使谷胱甘肽还原至正常水平。线粒体酶(例如异柠檬酸脱氢酶,α-酮戊二酸脱氢酶,琥珀酸脱氢酶和苹果酸脱氢酶)的活性在用ISO治疗的心肌缺血大鼠中显着降低,并且在用morin预处理后,这些酶的活性恢复了正常。此外,在ISO处理的大鼠中观察到细胞色素C氧化酶和NADH脱氢酶的活性降低,而用morin预处理可防止细胞色素C氧化酶和NADH脱氢酶的活性恢复正常。用morin预处理可将生化和功能参数恢复到接近正常水平,这表明morin对大鼠心脏线粒体功能具有抗ISO诱导的MI的显着保护作用。

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