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Voluntary wheel running abolishes vascular inflammation and restores endothelial function in old mice
Author(s) -
Connell Melanie L,
Durrant Jessica R,
Russell Molly J,
Donato Anthony J,
Seals Douglas R,
Lesniewski Lisa A
Publication year - 2009
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.23.1_supplement.777.6
Subject(s) - inflammation , tumor necrosis factor alpha , medicine , endocrinology , western blot , chemistry , proinflammatory cytokine , vascular smooth muscle , biochemistry , smooth muscle , gene
Aging is associated with impaired endothelial dependent dilation (EDD) and vascular inflammation. Aerobic exercise improves EDD in older humans and rodents, but it's unknown if this is associated with reduced vascular inflammation. Inflammatory cytokines were measured using multiplex ELISA in aortas of young (YC, 4‐6 mo) and old (OC, 29‐34 mo) cage‐control and old voluntary wheel running (OVR, 1.1±0.6 km/d, 12 wk) B6D2F1 mice (N=4‐6/group). EDD to acetylcholine was measured in isolated femoral arteries (N=6‐8/group). Interleukin‐1β (IL‐1β: 3.7±0.9 vs 1.6±0.5 pg/ml, P<0.05), interferon γ (IFNγ: 45.1±8.4 vs 15.0±5.0 pg/ml, P<0.05) and tumor necrosis factor a (TNF a: 2.6±0.5 vs 1.2±0.4 pg/ml, P<0.05) were higher and maximal EDD was lower (85±4% vs 97±3%, P<0.01) in OC vs. YC. In OVR, IL‐1β (1.1±0.7 pg/ml), IFNγ (26.5±2.0 pg/ml), TNF a (1.2±0.3 pg/ml) and EDD (95±2%) were restored to levels similar to or better than YC. To determine if the absence of vascular inflammation in OVR is associated with reduced activation of the pro‐inflammatory transcription factor, nuclear factor κ B (NFκB), we measured aortic protein expression of the inhibitor of NFκB, IκBa (western blot). IκBa was 117% greater in aortas of OVR compared with OC mice 1.3±0.3 vs 0.6±0.2 AUs, P<0.05). This is the first evidence that habitual exercise may restore the loss of EDD with aging by abolishing vascular inflammation, possibly via inhibition of NFκB. NIH AG013038 , AG006537 , AG015897 , AG029337 , AG000279