Amniotic membrane extracted proteins protect H9c2 cardiomyoblasts against hypoxia-induced apoptosis by modulating oxidative stress

Protection of the cardiac cell against hypoxia-induced cell damage is one of the main approaches to preventing cardiovascular disease. Earlier studies have shown the cardioprotective effect of the human Amniotic Membrane (hAM) in animal model of cardiac injury. However, the effect of Amniotic Membra...

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Bibliographic Details
Published in:Biochemical and biophysical research communications 2018-09, Vol.503 (3), p.1335-1341
Main Authors: Faridvand, Yousef, Nozari, Samira, Atashkhoei, Simin, Nouri, Mohammad, Jodati, Ahmadreza
Format: Article
Language:English
Subjects:
60 APPLIED LIFE SCIENCES
Amniotic Membrane Proteins
Apoptosis
CARDIOVASCULAR DISEASES
H9c2 cardiomyoblasts
Hypoxia
INFLAMMATION
MEMBRANE PROTEINS
Oxidative stress
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Summary:Protection of the cardiac cell against hypoxia-induced cell damage is one of the main approaches to preventing cardiovascular disease. Earlier studies have shown the cardioprotective effect of the human Amniotic Membrane (hAM) in animal model of cardiac injury. However, the effect of Amniotic Membrane Proteins (AMPs), extracted from hAM, on myocardial hypoxia injury remains unclear. So, our study aimed to investigate the protective effect of AMPs against hypoxia-induced cardiomyocytes apoptosis. H9c2 cardiomyocytes were pre-treated with AMPs followed by 24 h in hypoxia condition. Cell viability and apoptotic induction were detected by MTT and PI staining assay. Furthermore, the reactive oxygen species (ROS) generation, caspase-3 activity and malondialdehyde (MDA) were measured using the relevant kits. Moreover, apoptosis associated molecules and NF-kB p65 subunit, the master regulator of inflammation; expression was measured by western blotting. Our results indicated that AMPs increased the cellular viability of H9c2 cells during hypoxia and attenuated apoptotic induction. AMPs reduced hypoxia-induced ROS generation and as indicated by decreased MDA content. Moreover, AMPs decreased Bax/Bcl-2 ratios followed by reduction the caspase-3 activity; and further repressed the phosphorylated NF-kB p65. Altogether, suggesting that AMPs offers cardioprotective effects to H9c2 cell in hypoxia condition by modulating the gene involved in apoptosis and reducing oxidative stress and inflammatory response. •Hypoxia induces cell injury and apoptosis in H9c2 cells.•AMPs pre-treatment reinforce the antioxidant and anti-apoptosis properties in H9c2 cells against hypoxia.•AMPs regulate ROS balance, caspase 3 activation and Bcl2 family protein expression in H9c2 cells.
ISSN:0006-291X
1090-2104
DOI:10.1016/j.bbrc.2018.07.045