TAILIEUCHUNG - Cyclic nucleotides and mitogen-activated protein kinases: regulation of simvastatin in platelet activation

3-Hydroxy-3-methyl-glutaryl coenzyme A (HMG-CoA) reductase inhibitors (statins) have been widely used to reduce cardiovascular risk. These statins (., simvastatin) may exert other effects besides from their cholesterollowering actions, including inhibition of platelet activation. Platelet activation is relevant to a variety of coronary heart diseases. Although the inhibitory effect of simvastatin in platelet activation has been studied; the detailed signal transductions by which simvastatin inhibit platelet activation has not yet been completely resolved. Methods: The aim of this study was. | Lee et al. Journal of Biomedical Science 2010 17 45 http content 17 1 45 a NSC Tha cost of publication In Journal of Blomodlcal Science Is boms by tlM National Science Council Taiwan JOURNAL OF BIOMEDICAL SCIENCE RESEARCH Open Access Cyclic nucleotides and mitogen-activated protein kinases regulation of simvastatin in platelet activation Ye-Ming Lee21 2 Wei-Fan Chen23 Duen-Suey Chou 2 Thanasekaran Jayakumar3 Ssu-Yu Hou3 Jie-Jen Lee2 George Hsiao2 and Joen-Rong Sheu 2 3 Abstract Background 3-Hydroxy-3-methyl-glutaryl coenzyme A HMG-CoA reductase inhibitors statins have been widely used to reduce cardiovascular risk. These statins . simvastatin may exert other effects besides from their cholesterol-lowering actions including inhibition of platelet activation. Platelet activation is relevant to a variety of coronary heart diseases. Although the inhibitory effect of simvastatin in platelet activation has been studied the detailed signal transductions by which simvastatin inhibit platelet activation has not yet been completely resolved. Methods The aim of this study was to systematically examine the detailed mechanisms of simvastatin in preventing platelet activation. Platelet aggregation flow cytometric analysis immunoblotting and electron spin resonance studies were used to assess the antiplatelet activity of simvastatin. Results Simvastatin 20-50 UM exhibited more-potent activity of inhibiting platelet aggregation stimulated by collagen than other agonists . thrombin . Simvastatin inhibited collagen-stimulated platelet activation accompanied by Ca2 i mobilization thromboxane A2 TxA2 formation and phospholipase C PLC y2 protein kinase C PKC and mitogen-activated protein kinases . p38 MAPK JNKs phosphorylation in washed platelets. Simvastatin obviously increased both cyclic AMP and cyclic GMP levels. Simvastatin markedly increased NO release vasodilator-stimulated phosphoprotein VASP phosphorylation and endothelial nitric oxide synthase eNOS

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