Biochemical and Biophysical Research Communications
Heme oxygenase-1 induction may explain the antioxidant profile of aspirin☆
Section snippets
Methods
Materials. Fetal bovine serum, cell culture media, and penicillin–streptomycin were obtained from Gibco (Eggenstein, FRG). Tin protoporphyrin-IX (SnPP) was purchased from Alexis Deutschland GmbH (Grünberg, FRG). The Chemiluminescence Western blotting kit and anti-rabbit peroxidase-conjugated secondary antibody were from Boehringer Mannheim (Mannheim, FRG). All other chemicals were bought from Sigma (Deisenhofen, FRG).
Cell culture. Human endothelial cells derived from umbilical cord were
Endothelial cell viability
A 12-h pretreatment with aspirin protected endothelial cells from hydrogen peroxide-mediated toxicity, whereas indomethacin failed to exert a cytoprotective action (Fig. 1). Endothelial protection by aspirin was mimicked by exogenous bilirubin which led to an almost complete reversal of hydrogen peroxide-induced toxicity (Fig. 2). In order to explore a potential involvement of HO products such as bilirubin in the observed protection by aspirin, the HO inhibitor SnPP was used. At a concentration
Discussion
The beneficial cardiovascular effects of aspirin are generally attributed to its immediate platelet inhibitory function. However, accumulating evidence suggests that aspirin may have additional biological properties on the vasculature that contributes to the reduction of ischemic cardiovascular events in patients with hypertension and atherosclerosis [27], [28]. These possible nonplatelet-mediated effects include the attenuation of atherosclerosis due to inhibition of vascular smooth muscle
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Abbreviations: CO, carbon monoxide; HO, heme oxygenase; NO, nitric oxide; L-NAME, NG-nitro-l-arginine-methyl-ester; SnPP, tin protoporphyrin-IX.