Aspirin Reduces Endothelial Cell Senescence

The Durk Pearson & Sandy Shaw®
Life Extension NewsTM
Volume 8 No. 4 • October 2005

Aspirin Reduces Endothelial Cell Senescence

One of the consequences of aging is that more and more cells end up in a senescent state in which they are still viable and metabolically active but are unable to divide. Senescence has recently been discovered to be induced by oncogene (cancer-inducing gene) activation, thus supporting the theory that one function of senescence is to prevent the development of cancer.1

Although the senescent cells are alive and metabolically active, they do not function the same as nonsenescent cells.2 For example, the capacity of endothelial cells (which line blood vessels) to generate nitric oxide decreases in senescence.3 The suppression of oxidative stress or application of NO donors has been shown to delay the onset of replicative senescence in cell culture.3

The authors determined that when human umbilical-vein endothelial cells in culture were incubated with aspirin (100 µM), the activity of beta-galactosidase (a biomarker of senescence) was significantly decreased. In contrast to aspirin, ibuprofen and acetaminophen resulted in significant increases in beta-galactosidase activity. Addition of a nitric oxide synthase inhibitor (L-NAME) to the culture abolished the aspirin-reduced beta-galactosidase activity, demonstrating that the aspirin effect is mediated by nitric oxide.

Shortening of telomeres and decrease of telomerase is another mechanism that induces senescence. Aspirin increased telomerase activity significantly, compared to control, while ibuprofen and acetaminophen significantly reduced telomerase activity. Again, addition of the nitric oxide synthase inhibitor L-NAME to the culture with aspirin significantly blocked the effect of aspirin on telomerase activity, showing that nitric oxide mediates the effect.

The authors speculated, “It is conceivable and supported by recent observations that aspirin stimulates NO formation through its unique ability to trigger the synthesis of 15-epi-lipoxin A4. Aspirin is known to acetylate COX-2 within the endothelium, thus triggering 15-epi-lipoxin A4, which, in turn, elicits NO synthesis from both eNOS [endothelial nitric oxide synthase] and iNOS [inducible nitric oxide synthase].”3

We would expect this effect to be increased by use of an arginine supplement, especially if it contained choline and vitamin B5, because the latter two nutrients can be used to make acetylcholine, which activates eNOS conversion of arginine to nitric oxide.


  1. See, e.g., Braig et al. Oncogene-induced senescence as an initial barrier in lymphoma development. Nature 436:660-5 (2005); and Campisi. Suppressing cancer: the importance of being senescent. Science 309:886-7 (2005).
  2. See, e.g., Kletsas et al. The proinflammatory phenotype of senescent cells. Ann NY Acad Sci 1019:330-2 (2004).
  3. Bode-Boger et al. Aspirin reduces endothelial cell senescence. Biochem Biophys Res Commun 334:1226-32 (2005).

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