SIRT3 Mediates the Antioxidant Effect of Hydrogen Sulfide in Endothelial Cells
SIRT3
DOI:
10.1089/ars.2015.6331
Publication Date:
2015-09-30T10:38:17Z
AUTHORS (19)
ABSTRACT
Oxidative stress is a key contributor to endothelial dysfunction and associated cardiovascular pathogenesis. Hydrogen sulfide (H2S) an antioxidant gasotransmitter that protects cells against oxidative stress. Sirtuin3 (SIRT3), which belongs the silent information regulator 2 (SIR2) family, important deacetylase under H2S able regulate activity of several sirtuins. The present study aims investigate role SIRT3 in effect cells.Cultured EA.hy926 were exposed hydrogen peroxide (H2O2) as model stress-induced cell injury. GYY4137, slow-releasing donor, improved viability, reduced apoptosis, mitochondrial function following H2O2 treatment. reversed stimulation MAPK phosphorylation, downregulation mRNA reduction superoxide dismutase isocitrate dehydrogenase expression induced by H2O2. also increased activator protein 1 (AP-1) binding with promoter this was absent presence specific AP-1 inhibitor, SR11302 or curcumin. Paraquat administration mice defected endothelium-dependent aortic vasodilatation both mouse aorta small mesenteric artery, alleviated GYY4137 This vasoprotective knockout mice.The results highlight novel for protective oxidant damage endothelium vitro vivo.H2S enhances promoter, thereby upregulating ultimately reducing oxidant-provoked vascular dysfunction. Antioxid. Redox Signal. 24, 329-343.
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