The Durk Pearson & Sandy Shaw®
Life Extension NewsTM
Volume 11 No. 6 • October 2008


New Blades Added to the Swiss Army Knife of Preventive Medicine: Aspirin

New discoveries on the effects of aspirin (the acetylated version of the plant hormone salicylic acid) keep adding new understanding of the mechanisms for its health benefits. A newly published paper1 explains more on the source of cardiovascular protection by aspirin by revealing that aspirin induced paraoxonase 1 (PON1, a molecule that is synthesized in the liver and circulates in association with apo-A1 and HDL) and the apo-A1 gene in mice.

PON1 is a known protectant against atherosclerosis; studies have shown that people who take aspirin have increased levels of PON1. PON1-deficient mice have been shown to be more susceptible to atherosclerosis.1 Moreover, low levels of HDL are positively correlated with low levels of PON1.1 The cardiovascular protective effects of HDL depend to a great extent on its content of apoA1 and PON1. The fact that HDL becomes less protective and even proatherogenic due to oxidative- and/or nitrative-stress-induced damage to apoA1 and PON1 in those with cardiovascular disease or risk factors for it is probably one of the major reasons that it is not uncommon for people with normal levels of HDL and LDL to still have heart attacks.

In this study,1 normal C57BL/6 mice were fed 2 mg/day or not of aspirin along with an atherogenic diet for 9 days. The aspirin-fed mice had a 10-fold induction in PON1 liver gene expression and a 6-fold induction in apoA-1 gene expression compared with the controls (not receiving aspirin).

Interestingly, a number of natural substances have also been found to increase PON1, including quercetin and catechin (in both humans and mice); resveratrol was reported to induce PON1 gene expression in primary hepatocyte (liver cells) culture.1

Reference

  1. Jaichander et al. Induction of paraoxonase 1 and apolipoprotein A-1 gene expression by aspirin. J Lipid Res 49:2142-8 (2008).

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