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En Face Detection of Nitric Oxide and Superoxide in Endothelial Layer of Intact Arteries
Published on: February 25, 2016
Superoxide-lowering therapy with TEMPOL reverses arterial dysfunction with aging in mice
Bradley S Fleenor1, Douglas R Seals, Melanie L Zigler
1Department of Integrative Physiology, University of Colorado, Boulder, CO 80309, USA. bradley.fleenor@colorado.edu
Aging Cell
|December 16, 2011
Summary
The antioxidant TEMPOL significantly improved arterial aging in mice by reducing aortic stiffening and restoring endothelial function. This study shows TEMPOL
Area of Science:
- Cardiovascular Science
- Aging Research
- Biochemistry
Background:
- Arterial aging is characterized by stiffening and endothelial dysfunction.
- Oxidative stress, particularly increased superoxide levels, contributes to age-related vascular changes.
- Superoxide dismutase (SOD) enzymes play a crucial role in mitigating oxidative stress.
Purpose of the Study:
- To investigate the efficacy of TEMPOL, a superoxide dismutase mimetic, in ameliorating age-related arterial dysfunction.
- To determine the impact of TEMPOL on aortic stiffening, endothelial function, and associated molecular markers in aged mice.
Main Methods:
- Young and old male C57BL6 mice were treated with TEMPOL or placebo for 3 weeks.
- Aortic pulse wave velocity (aPWV) and acetylcholine-stimulated endothelium-dependent dilation (EDD) were measured.
- Arterial superoxide levels, collagen I expression, nitric oxide (NO) bioavailability, endothelial NO synthase (eNOS) expression, nitrotyrosine, NADPH oxidase, and pro-inflammatory cytokines were assessed.
Main Results:
- Old mice exhibited increased aortic superoxide, arterial stiffening (higher aPWV), and impaired endothelial function (reduced EDD) compared to young mice.
- TEMPOL treatment normalized aortic superoxide, reversed arterial stiffening, and restored endothelial function in old mice.
- TEMPOL also normalized collagen I expression, enhanced NO bioavailability, increased eNOS expression, reduced oxidative stress markers (nitrotyrosine, NADPH oxidase), and decreased pro-inflammatory cytokines.
Conclusions:
- Short-term TEMPOL treatment effectively ameliorates large elastic artery stiffening and endothelial dysfunction associated with aging in mice.
- The beneficial effects of TEMPOL are linked to the normalization of arterial collagen I, eNOS, oxidative stress, and inflammation.
- TEMPOL represents a potential therapeutic strategy for combating age-related vascular decline.