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

Abstract 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...

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Bibliographic Details
Published in:Free radical research 2014-05, Vol.48 (5), p.526-533
Main Authors: Cannizzo, B., Quesada, I., Militello, R., Amaya, C., Miatello, R., Cruzado, M., Castro, C.
Format: Article
Language:English
Subjects:
Animals
atherosclerosis
Atherosclerosis - etiology
Atherosclerosis - metabolism
Cyclic N-Oxides - adverse effects
Inflammation - metabolism
Male
Metabolic Syndrome - complications
Mice
Mice, Inbred C57BL
NADPH oxidase
NADPH Oxidases - metabolism
Oxidative Stress
Reactive Oxygen Species
Spin Labels
tempol
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Summary:Abstract 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 (ApoE-KO) mice. Rodents were fed with fructose overload (FF, 10% w/v) for 8 weeks and treated with Tempol 1 mg/kg/day 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 1 (VCAM-1) 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 with metabolic syndrome.
ISSN:1071-5762
1029-2470
DOI:10.3109/10715762.2014.889295