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Abstract : |
This study was conducted to investigate the effects of nimesulide in platelet aggregation. It shows that nimesulide (1-100 M) inhibited platelets aggregation induced by adrenaline, (20-200 M). It also inhibed thromboxane A2 (TXA2) formation by platelets at low concentration (IC50; 1M). However, much lower concentrations of nimesulide (0.01-0.1 M) potentiated the aggregatory response of subthreshold concentrations of adrenaline (0.2-2 M). Such an effect was blocked by Ca2+-channel blockers, verapamil and diltiazem (IC50: 7 and 46 M, respectively), nitric oxide donor, SNAP (IC50: 2 M) and cinchonine (10 nM) but not by genistein (up to 10 M). These results are indicative of the concentration-dependent dual effects of nimesulide on human platelet aggregation. The synergistic effect of low doses of nimesulide and adrenaline seems to be mediated through inhibition of multiple signaling pathways. , This study was conducted to investigate the effects of nimesulide in platelet aggregation. It shows that nimesulide (1-100 أƒإ½أ‚آ¼ M) inhibited platelets aggregation induced by adrenaline, (20-200 أƒإ½أ‚آ¼ M). It also inhibed thromboxane A2 (TXA2) formation by platelets at low concentration (IC50; 1 أƒإ½أ‚آ¼ M). However, much lower concentrations of nimesulide (0.01-0.1 أƒإ½أ‚آ¼ M) potentiated the aggregatory response of subthreshold concentrations of adrenaline (0.2-2 أƒإ½أ‚آ¼ M). Such an effect was blocked by Ca2+-channel blockers, verapamil and diltiazem (IC50: 7 and 46 أƒإ½أ‚آ¼ M, respectively), nitric oxide donor, SNAP (IC50: 2 أƒإ½أ‚آ¼ M) and cinchonine (10 nM) but not by genistein (up to 10 أƒإ½أ‚آ¼ M). These results are indicative of the concentration-dependent dual effects of nimesulide on human platelet aggregation. The synergistic effect of low doses of nimesulide and adrenaline seems to be mediated through inhibition of multiple signaling pathways., |
