首页> 外文期刊>International Journal of Cardiology >Ganoderma lucidum ameliorate mitochondrial damage in isoproterenol-induced myocardial infarction in rats by enhancing the activities of TCA cycle enzymes and respiratory chain complexes
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Ganoderma lucidum ameliorate mitochondrial damage in isoproterenol-induced myocardial infarction in rats by enhancing the activities of TCA cycle enzymes and respiratory chain complexes

机译:灵芝通过增强TCA循环酶和呼吸链复合物的活性来减轻异丙肾上腺素诱发的大鼠心肌梗死的线粒体损伤

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Background: Decreased mitochondrial function has been suggested to be one of the important pathological events in isoproterenol (ISO)-induced cardiotoxicity. In this communication, we have evaluated the protective effect of Ganoderma lucidum against ISO induced cardiac toxicity and mitochondrial dysfunction. Methods: Cardiac toxicity was assessed by determining the activities of creatine kinase (CK) and lactate dehydrogenases (LDH) after subcutaneous injection of ISO (85 mg/kg) at an interval of 24 h for 2 days. The animals were sacrificed 24 h after last ISO administration. G. lucidum (100 and 250 mg/kg, p.o.) was given to the rats once daily for 15 days prior to the ISO challenge. Similarly, α-Tocopherol (100 mg/kg, p.o) was kept as the standard. To assess the extent of cardiac mitochondrial damage, the activities of Krebs cycle dehydrogenases and mitochondrial complexes I, II, III, and IV as well as the level of ROS and mitochondrial membrane potential (ΔΨmt) were evaluated. Results: Administration of G. lucidum and α-tocopherol significantly protected the elevated activities of CK and LDH. Further, the activities of mitochondrial enzymes and the level of ΔΨmt were significantly enhanced and the level of ROS was significantly declined in the G. lucidum and α-tocopherol treatments. Conclusion: The present study concluded that the cardiac mitochondrial enzymes are markedly declined by the ISO challenge and the administration G. lucidum and α-Tocopherol significantly protected mitochondria by preventing the decline of antioxidant status and ΔΨmt or by directly scavenging the free radicals.
机译:背景:线粒体功能降低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之一。在本通讯中,我们评估了灵芝对ISO诱导的心脏毒性和线粒体功能障碍的保护作用。方法:在皮下注射ISO(85 mg / kg)间隔24小时连续2天后,通过测定肌酸激酶(CK)和乳酸脱氢酶(LDH)的活性来评估心脏毒性。最后一次ISO施用后24小时处死动物。在ISO攻击之前,每天一次给大鼠一次灵芝(100和250 mg / kg,p.o。),持续15天。同样,以α-生育酚(100 mg / kg,口服)为标准。为了评估心脏线粒体的损​​伤程度,评估了克雷布斯循环脱氢酶和线粒体复合体I,II,III和IV的活性,以及​​ROS和线粒体膜电位(ΔΨmt)的水平。结果:灵芝和α-生育酚的施用显着保护了CK和LDH的升高的活性。此外,在灵芝和α-生育酚处理中,线粒体酶的活性和ΔΨmt的水平显着提高,并且ROS的水平显着下降。结论:本研究的结论是,ISO挑战显着降低了心脏线粒体酶,G。lucidum和α-生育酚的给药通过防止抗氧化剂状态和ΔΨmt的下降或直接清除自由基来显着保护线粒体。

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