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

Li, Wenjuan; Nie, Shaoping; Yan, Yan; Zhu, Shang-Bin; Xie, Mingyong

doi:10.1016/j.lfs.2009.09.001

Cited by 25 publications

(11 citation statements)

References 36 publications

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“…Cardiac tissue is highly susceptible to oxidative damage, because cardiomyocytes are rich in mitochondria, the site of basal ROS generation, and are also exposed to relatively high oxygen tension compared to other tissues (27). The first line of cell defense against oxidative stress-mediated cardiac injury comprises several endogenous antioxidant enzymes such as MnSOD, catalase, and glutathione peroxidase, which act together to scavenge ROS.…”

Section: Discussionmentioning

confidence: 99%

A Major Green Tea Component, (−)-Epigallocatechin-3-gallate, Ameliorates Doxorubicin-Mediated Cardiotoxicity in Cardiomyocytes of Neonatal Rats

Nie

Xie

et al. 2010

J. Agric. Food Chem.

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Cardiac injury is a major complication of the oxidative stress-generating anticancer drug doxorubicin (DOX). The green tea polyphenol (-)-epigallocatechin-3-gallate (EGCG) has been reported to play a cardioprotective role in diseases associated with oxidative stress. The objective of this study was to investigate whether EGCG can protect against DOX-induced toxicity in cardiomyocytes. The data showed that EGCG protected the cardiomyocytes from DOX-mediated cardiotoxicity, as evidenced by decreased lactate dehydrogenase (LDH) activity and increased cell viability in a dose-dependent manner. EGCG treatment also decreased malondialdehyde content and increased protein expression and activities of manganese superoxide dismutase (MnSOD), catalase, and glutathione peroxidase. Furthermore, treatment with EGCG decreased reactive oxygen species (ROS) production and apoptosis. This study suggests that EGCG could protect cardiomyocytes from DOX-induced oxidative stress by attenuating ROS production, apoptosis, and increasing activities and protein expression of endogenous antioxidant enzymes.

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Section: Discussionmentioning

confidence: 99%

A Major Green Tea Component, (−)-Epigallocatechin-3-gallate, Ameliorates Doxorubicin-Mediated Cardiotoxicity in Cardiomyocytes of Neonatal Rats

Nie

Xie

et al. 2010

J. Agric. Food Chem.

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“…5-Bromo-2′-deoxyuridine (100 µM) was added during the first 48 hours to inhibit non-myocyte proliferation. Simulated I/R (SI/R) was employed as previously described [23]. Briefly, simulated ischemia buffer (composition in mM: NaCl 98.5, KCl 10, MgSO 4 1.2, CaCl 2 1.0, HEPES 20, sodium lactate 40, pH 6.8) and simulated reoxygenation buffer (composition in mM: NaH 2 PO 4 0.9, NaHCO 3 20.0, CaCl 2 1.0, MgSO 4 1.2, HEPES 20.0, NaCl 129.5, KCl 5.0, glucose 5.5, pH 7.4) were prepared in advance.…”

Section: Methodsmentioning

confidence: 99%

Ginsenoside Rd Attenuates Myocardial Ischemia/Reperfusion Injury via Akt/GSK-3β Signaling and Inhibition of the Mitochondria-Dependent Apoptotic Pathway

Wang

et al. 2013

PLoS ONE

103

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Evidence suggests Ginsenoside Rd (GSRd), a biologically active extract from the medical plant Panax Ginseng, exerts antioxidant effect, decreasing reactive oxygen species (ROS) formation. Current study determined the effect of GSRd on myocardial ischemia/reperfusion (MI/R) injury (a pathological condition where ROS production is significantly increased) and investigated the underlying mechanisms. The current study utilized an in vivo rat model of MI/R injury and an in vitro neonatal rat cardiomyocyte (NRC) model of simulated ischemia/reperfusion (SI/R) injury. Infarct size was measured by Evans blue/TTC double staining. NRC injury was determined by MTT and lactate dehydrogenase (LDH) leakage assay. ROS accumulation and apoptosis were assessed by flow cytometry. Mitochondrial membrane potential (MMP) was determined by 5, 5′, 6, 6′-tetrachloro-1, 1′, 3, 3′-tetrathylbenzimidazol carbocyanine iodide (JC-1). Cytosolic translocation of mitochondrial cytochrome c and expression of caspase-9, caspase-3, Bcl-2 family proteins, and phosphorylated Akt and GSK-3β were determined by western blot. Pretreatment with GSRd (50 mg/kg) significantly augmented rat cardiac function, as evidenced by increased left ventricular ejection fraction (LVEF) and ±dP/dt. GSRd reduced myocardial infarct size, apoptotic cell death, and blood creatine kinase/lactate dehydrogenase levels after MI/R. In NRCs, GSRd (10 µM) inhibited SI/R-induced ROS generation (P<0.01), decreased cellular apoptosis, stabilized the mitochondrial membrane potential (MMP), and attenuated cytosolic translocation of mitochondrial cytochrome c. GSRd inhibited activation of caspase-9 and caspase-3, increased the phosphorylated Akt and GSK-3β, and increased the Bcl-2/Bax ratio. Together, these data demonstrate GSRd mediated cardioprotective effect against MI/R–induced apoptosis via a mitochondrial-dependent apoptotic pathway.

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“…Total proteins were extracted from the pancreatic tissues and electro-transphoresed on a 12% SDS-PAGE gel, and then they were transferred to a nitrocellulose membrane according to method of Li, et al [21]. β-actin was used to normalize loading variations.…”

Section: Biochemical Assays and Western Blotmentioning

confidence: 99%

Effects of Ganoderma lucidum polysaccharides on chronic pancreatitis and intestinal microbiota in mice

Zhuo

Teng

et al. 2016

International Journal of Biological Macromolecules

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

Cited by 25 publications

References 36 publications

A Major Green Tea Component, (−)-Epigallocatechin-3-gallate, Ameliorates Doxorubicin-Mediated Cardiotoxicity in Cardiomyocytes of Neonatal Rats

A Major Green Tea Component, (−)-Epigallocatechin-3-gallate, Ameliorates Doxorubicin-Mediated Cardiotoxicity in Cardiomyocytes of Neonatal Rats

Ginsenoside Rd Attenuates Myocardial Ischemia/Reperfusion Injury via Akt/GSK-3β Signaling and Inhibition of the Mitochondria-Dependent Apoptotic Pathway

Effects of Ganoderma lucidum polysaccharides on chronic pancreatitis and intestinal microbiota in mice

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