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The protective effect of Ganoderma atrum polysaccharide against anoxia/reoxygenation injury in neonatal rat cardiomyocytes.

机译:灵芝多糖对新生大鼠心肌细胞缺氧/复氧损伤的保护作用。

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AIMS: Oxidative stress has been largely implicated in the pathogenesis of anoxia/reoxygenation injury. Ganoderma atrum polysaccharide (PSG-1), the most abundant component extracted from the fruiting bodies of G. atrum, has been shown to possess potent antioxidant activity. In this study, we investigated whether PSG-1 attenuates oxidative stress induced by anoxia/reoxygenation injury. MAIN METHODS: Primary cultures of neonatal rat cardiomyocytes pretreated with PSG-1 were exposed to anoxia/reoxygenation and subsequently monitored for cell viability by the MTT assay. Lactate dehydrogenase (LDH) release, manganese superoxide dismutase (MnSOD), catalase and glutathione peroxidase activities, and malondialdehyde contents were determined by a colorimetric method. The levels of reactive oxygen species (ROS) and apoptosis were determined by flow cytometry. Western blot analysis was used for the determination of MnSOD, catalase and glutathione peroxidase expression. KEY FINDINGS: In the present study, PSG-1 protected the cardiomyocytes from anoxia/reoxygenation injury, as evidenced by decreased LDH release and increased cell viability in a dose-dependent manner up to 100microg/ml. This protective effect concomitantly decreased malondialdehyde contents, while significantly increased the activities and protein expressions of MnSOD, catalase and glutathione peroxidase. Furthermore, treatment with PSG-1 decreased ROS production and apoptosis in cardiomyocytes undergoing anoxia/reoxygenation. SIGNIFICANCE: The present study first demonstrates that PSG-1 protects cardiomyocytes against oxidative stress induced by anoxia/reoxygenation by attenuating ROS production, apoptosis and increasing activities and protein expressions of endogenous antioxidant enzymes.
机译:目的:氧化应激在很大程度上涉及缺氧/复氧损伤的发病机理。从灵芝子实体中提取的最丰富的成分灵芝灵芝多糖(PSG-1)已显示具有有效的抗氧化活性。在这项研究中,我们调查了PSG-1是否减轻由缺氧/复氧损伤引起的氧化应激。主要方法:将经过PSG-1预处理的新生大鼠心肌细胞的原代培养物暴露于缺氧/复氧状态,然后通过MTT分析监测细胞活力。用比色法测定乳酸脱氢酶(LDH)的释放,锰超氧化物歧化酶(MnSOD),过氧化氢酶和谷胱甘肽过氧化物酶的活性以及丙二醛含量。通过流式细胞仪测定活性氧(ROS)和凋亡的水平。蛋白质印迹分析用于确定MnSOD,过氧化氢酶和谷胱甘肽过氧化物酶的表达。关键发现:在本研究中,PSG-1保护心肌细胞免受缺氧/复氧损伤,如LDH释放减少和细胞生存力以剂量依赖性方式增加直至100microg / ml所证明。这种保护作用同时降低了丙二醛含量,同时显着增加了MnSOD,过氧化氢酶和谷胱甘肽过氧化物酶的活性和蛋白质表达。此外,用PSG-1进行治疗可降低经历缺氧/复氧的心肌细胞中ROS的产生和凋亡。意义:本研究首先证明PSG-1可通过减轻ROS的产生,凋亡以及增加内源性抗氧化酶的活性和蛋白表达来保护心肌细胞免受缺氧/复氧诱导的氧化应激。

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