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.
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http://dx.doi.org/10.1016/j.lfs.2009.09.001 | DOI Listing |
Chin Med J (Engl)
January 2025
Key Laboratory of Hepatosplenic Surgery, Ministry of Education, Department of Minimal Invasive Hepatic Surgery, The First Affiliated Hospital of Harbin Medical University, Harbin, Heilongjiang 150001, China.
Background: Arsenic trioxide (ATO) is indicated as a broad-spectrum medicine for a variety of diseases, including cancer and cardiac disease. While the role of ATO in hepatic ischemia/reperfusion injury (HIRI) has not been reported. Thus, the purpose of this study was to identify the effects of ATO on HIRI.
View Article and Find Full Text PDFSci Rep
January 2025
Department of Cardiovascular Surgery, The First Affiliated Hospital, Jiangxi Medical College, Nanchang University, 17 Yongwai Road, Nanchang, 330006, Jiangxi, China.
The study aimed to elucidate the underlying pharmacological mechanism of the traditional Chinese medicine Pue in ameliorating myocardial ischemia-reperfusion injury (MIRI), a critical clinical challenge exacerbated by reperfusion therapy. In vivo MIRI and in vitro anoxia/reoxygenation (A/R) models were constructed. The results demonstrated that Pue pretreatment effectively alleviated MIRI, as manifested by diminishing the levels of serum CK-MB and LDH, mitigating the extent of myocardial infarction and enhancing cardiac functionality.
View Article and Find Full Text PDFInt J Mol Med
December 2024
Department of Cardiovascular Surgery, The First Affiliated Hospital, Jiangxi Medical College, Nanchang University, Nanchang, Jiangxi 330006, P.R. China.
J Biochem Mol Toxicol
October 2024
Department of Nephrology, Faculty of Medicine, University of Thessaly, Larissa, Greece.
Ischemia-reperfusion (I-R) injury is the most common cause of acute kidney injury. In experiments involving primary human renal proximal tubular epithelial cells (RPTECs) exposed to anoxia-reoxygenation, we explored the hypothesis that mitochondrial malate dehydrogenase-2 (MDH-2) inhibition redirects malate metabolism from the mitochondria to the cytoplasm, towards the malate-pyruvate cycle and reversed malate-aspartate shuttle. Colorimetry, fluorometry, and western blotting showed that MDH2 inhibition accelerates the malate-pyruvate cycle enhancing cytoplasmic NADPH, thereby regenerating the potent antioxidant reduced glutathione.
View Article and Find Full Text PDFExp Ther Med
September 2024
Department of Thoracic and Cardiovascular Surgery, Nanjing First Hospital, Nanjing Medical University, Nanjing, Jiangsu 210006, P.R. China.
Ischemic heart disease (IHD) remains a leading cause of mortalities worldwide, necessitating timely reperfusion to reduce acute mortality. Paradoxically, reperfusion can induce myocardial ischemia/reperfusion (I/R) injury, which is primarily characterized by mitochondrial dysfunction. Translocator protein (TSPO) participates in multiple cellular events; however, its role in IHD, especially in the process of myocardial I/R injury, has not been well determined.
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