Aspirin reduces endothelial cell senescence

Stefanie M. Bode-Böger, Jens Martens-Lobenhoffer, Michael Täger, Henning Schröder, Fortunato Scalera

Research output: Contribution to journalArticlepeer-review

80 Scopus citations


We report here the effect of aspirin on the onset of replicative senescence. Endothelial cells that were cultured until cumulative population doublings 40 showed clear signs of aging. Incubation with aspirin inhibited senescence-associated β-galactosidase activity and increased telomerase activity. Along with the delayed onset of senescence, aspirin decreased reactive oxygen species and increased nitric oxide (NO) and cGMP levels. Furthermore, aspirin reduced the elaboration of asymmetric dimethylarginine (ADMA), an endogenous inhibitor of NO synthase, and up-regulated the activity of dimethylarginine dimethylaminohydrolase, the enzyme that degrades ADMA. These effects were specific in that other nonsteroidal anti-inflammatory drugs, such as ibuprofen or acetaminophen, did not prevent the onset of endothelial senescence. The NO synthase inhibitor l-NAME, but not its inactive d-enantiomer, led to complete inhibition of aspirin-delayed senescence. These findings demonstrate that aspirin delays the onset of endothelial senescence by preventing a decrease in NO formation/generation. This might provide a therapeutic strategy aimed at blocking aging-induced NO inhibition.

Original languageEnglish (US)
Pages (from-to)1226-1232
Number of pages7
JournalBiochemical and Biophysical Research Communications
Issue number4
StatePublished - Sep 9 2005

Bibliographical note

Copyright 2008 Elsevier B.V., All rights reserved.


  • Aging
  • Aspirin
  • Asymmetric dimethylarginine
  • Dimethylarginine dimethylaminohydrolase
  • L-NAME
  • Nitric oxide
  • Oxidative stress
  • Reactive oxygen species
  • Senescence
  • Telomerase


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