Aspirin inhibits inducible nitric oxide synthase expression and tumour necrosis factor-alpha release by cultured smooth muscle cells

Background Inflammatory related cardiovascular disease, i.e. cardiac allogr aft rejection, myocarditis, septic shock, are accompanied by cytokine produ ction, which stimulates the expression of inducible nitric oxide (iNOS). Materials and methods The aim of the present study was to examine whether a ntiinflammatory doses of acetylsalicylic acid (aspirin) could regulate iNOS protein expression in bovine vascular smooth muscle cells (BVSMCs) in cult ure. Results Interleukin 1 beta (IL-1 beta, 0.03 U mL(-1)) induced nitric oxide release by BVSMCs. Aspirin inhibited nitric oxide release from IL-1 beta-st imulated BVSMCs in a dose-dependent manner. In addition, aspirin significan tly inhibited iNOS protein expression in BVSMCs and reduced the translocati on of the nuclear factor-kappa B (NF-kappa B). Furthermore, aspirin and the blockade of NO generation by BVSMCs reduced the production of tumour necro sis factor alpha (TNF-alpha) by these cells. Conclusion High doses of aspirin inhibited iNOS protein expression in BVSMC s and decreased NF-kappa B mobilization. The inhibition of iNOS expression by aspirin was further associated with a reduced ability of BVSMCs to produ ce TNF-alpha. This study could provide new mechanisms of action for aspirin in the treatment of the inflammation-related cardiovascular diseases.