Redox-sensitive regulation of macrophage-inducible nitric oxide synthase expression in vitro does not correlate with the failure of apocynin to prevent lung inflammation induced by endotoxin

0370393 - BFÚ 2012 RIV DE eng J - Journal Article
Viačková, Daniela - Pekarová, Michaela - Crhák, Tomáš - Búcsaiová, M. - Matiašovic, J. - Lojek, Antonín - Kubala, Lukáš
Redox-sensitive regulation of macrophage-inducible nitric oxide synthase expression in vitro does not correlate with the failure of apocynin to prevent lung inflammation induced by endotoxin.
Immunobiology. Roč. 216, č. 4 (2011), s. 457-465. ISSN 0171-2985
R&D Projects: GA ČR(CZ) GA524/06/1197; GA ČR(CZ) GA524/08/1753
Institutional research plan: CEZ:AV0Z50040507; CEZ:AV0Z50040702
Keywords : lung inflammation * reactive oxygen species * phagocytes
Subject RIV: BO - Biophysics
Impact factor: 3.205, year: 2011

The aim was to evaluate the potential of selected antioxidants or inhibitors of NADPH oxidase (glutathione, N-acetyl cysteine, trolox, apocynin, and diphenyleneiodonium chloride) to modulate nitric oxide (NO) production and inducible nitric oxide synthase (iNOS) expression by mouse macrophages induced by lipopolysaccharide (LPS) in vitro and to evaluate the potential of apocynin to modulate the course of LPS-induced lung inflammation in vivo. Our data suggest that the inhibitors of NADPH oxidase possess inhibitory potential against LPS-induced NO production by mouse macrophages; however, apocynin failed to reduce LPS-induced lung inflammation in mice.
Permanent Link: http://hdl.handle.net/11104/0204215