Tempol attenuates atherosclerosis associated with metabolic syndrome via decreased vascular inflammation and NADPH-2 oxidase expression

CANNIZZO, B AND QUESADA, I; MILITELLO, RD; AMAYA, C; MIATELO, R; CRUZADO, M; CASTRO, C

FREE RADICAL RESEARCH

TAYLOR & FRANCIS LTD

Lugar: Londres; Año: 2014 p. 3109 - 3119

1071-5762

Oxidative stress is an important factor in the generation of vascular injury in atherosclerosis. Chronic administration of fructose in rodents is able to facilitate oxidative damage. In the present study we evaluated the role of Tempol, a superoxide dismutase mimetic, on the effect of high fructose intake in apolipoprotein E-deficient mice (ApoE-KO). Mice were fed with fructose overload (FF, 10% w / v) for 8 weeks and treated with Tempol 1 mg/kg the latest 4 weeks. Tempol revert the pro-oxidant effects caused by FF, diminished lipid peroxidation and impaired vascular NADPH oxidase system through the downregulation of p47phox expression in the vascular wall. Tempol inhibited the expression of vascular adhesion molecule (VCAM) in aorta and reduced the development of atheroma plaques. Our results indicate that tempol attenuates oxidative stress by interfering with the correct assembly of Nox2 oxidase complex in the vascular wall and is able to reduce atherosclerosis. Thus tempol represents a potential therapeutic target for preventing risk factors associated to metabolic syndrome.