Cardioprotective mechanism of S-nitroso-N-acetylcysteine via S-nitrosated betadrenoceptor-2 in the LDLr−/− mice

•We model a dyslipidemic LDLr−/− mice which have LVH after 15days on a HFD.•We have shown that SNAC treatment suppress cardiac remodeling in this model.•We examine the ability of SNAC to modulate oxidative stress during LVH.•SNAC decreases oxidative stress levels by decreasing H2O2 and O2- productio...

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Veröffentlicht in:	Nitric oxide 2014-01, Vol.36, p.58-66
Hauptverfasser:	Wanschel, Amarylis Claudine Bonito Azeredo, Caceres, Viviane Menezes, Moretti, Ana Iochabel Soares, Bruni-Cardoso, Alexandre, de Carvalho, Hernandes Faustino, de Souza, Heraldo Possolo, Laurindo, Francisco Rafael Martins, Spadari, Regina Célia, Krieger, Marta Helena
Format:	Artikel
Sprache:	eng
Schlagworte:	Acetylcysteine - analogs & derivatives Acetylcysteine - pharmacology Animals Antioxidants - pharmacology Apoptosis Betadrenoceptor-2 Dyslipidemias Endoplasmic Reticulum - metabolism Gene Expression Regulation Hydrogen peroxide Hydrogen Peroxide - chemistry Hypertrophy, Left Ventricular Male Mice Mice, Inbred C57BL Mice, Knockout Myocytes, Cardiac - cytology Nitric Oxide Synthase Type III - metabolism Nitrogen - metabolism Oxidative Stress Reactive Oxygen Species - metabolism Receptors, Adrenergic, beta-2 - genetics Receptors, LDL - genetics S-nitrosated S-nitroso-N-acetylscysteine Superoxide Superoxides Ventricular hypertrophy
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