Department of Biochemistry and Biotechnology, Annamalai University, Annamalai nagar, 608002, Tamil Nadu, India.
Cell Stress Chaperones. 2010 Nov;15(6):791-806. doi: 10.1007/s12192-010-0187-9. Epub 2010 Apr 9.
Cardiac mitochondrial dysfunction plays an important role in the pathology of myocardial infarction. The protective effects of caffeic acid on mitochondrial dysfunction in isoproterenol-induced myocardial infarction were studied in Wistar rats. Rats were pretreated with caffeic acid (15 mg/kg) for 10 days. After the pretreatment period, isoproterenol (100 mg/kg) was subcutaneously injected to rats at an interval of 24 h for 2 days to induce myocardial infarction. Isoproterenol-induced rats showed considerable increased levels of serum troponins and heart mitochondrial lipid peroxidation products and considerable decreased glutathione peroxidase and reduced glutathione. Also, considerably decreased activities of isocitrate, succinate, malate, α-ketoglutarate, and NADH dehydrogenases and cytochrome-C-oxidase were observed in the mitochondria of myocardial-infarcted rats. The mitochondrial calcium, cholesterol, free fatty acids, and triglycerides were considerably increased and adenosine triphosphate and phospholipids were considerably decreased in isoproterenol-induced rats. Caffeic acid pretreatment showed considerable protective effects on all the biochemical parameters studied. Myocardial infarct size was much reduced in caffeic acid pretreated isoproterenol-induced rats. Transmission electron microscopic findings also confirmed the protective effects of caffeic acid. The possible mechanisms of caffeic acid on cardiac mitochondria protection might be due to decreasing free radicals, increasing multienzyme activities, reduced glutathione, and adenosine triphosphate levels and maintaining lipids and calcium. In vitro studies also confirmed the free-radical-scavenging activity of caffeic acid. Thus, caffeic acid protected rat's heart mitochondria against isoproterenol-induced damage. This study may have a significant impact on myocardial-infarcted patients.
心肌线粒体功能障碍在心肌梗死的病理学中起着重要作用。本研究旨在探讨咖啡酸对异丙肾上腺素诱导的心肌梗死大鼠心肌线粒体功能障碍的保护作用。Wistar 大鼠预先用咖啡酸（15mg/kg）处理 10 天。预处理期后，每隔 24 小时给大鼠皮下注射异丙肾上腺素（100mg/kg），连续 2 天诱导心肌梗死。异丙肾上腺素诱导的大鼠血清肌钙蛋白和心肌线粒体脂质过氧化产物显著增加，谷胱甘肽过氧化物酶和还原型谷胱甘肽显著减少。此外，心肌梗死大鼠的线粒体中还观察到异柠檬酸、琥珀酸、苹果酸、α-酮戊二酸和 NADH 脱氢酶以及细胞色素-C-氧化酶的活性显著降低。异丙肾上腺素诱导的大鼠线粒体钙、胆固醇、游离脂肪酸和甘油三酯显著增加，三磷酸腺苷和磷脂显著减少。咖啡酸预处理对所有研究的生化参数均显示出显著的保护作用。与异丙肾上腺素诱导的大鼠相比，咖啡酸预处理大鼠的心肌梗死面积明显减小。透射电子显微镜观察结果也证实了咖啡酸的保护作用。咖啡酸对心肌线粒体的保护作用的可能机制是通过减少自由基、增加多种酶的活性、增加还原型谷胱甘肽和三磷酸腺苷水平以及维持脂质和钙。体外研究也证实了咖啡酸清除自由基的活性。因此，咖啡酸可保护大鼠心脏线粒体免受异丙肾上腺素诱导的损伤。这项研究可能对心肌梗死患者有重要影响。
