Effects of Selenium in the MAPK Signaling Cascade

Introduction: this study aimed to discover by which mechanism selenium (se) suppresses stimulated platelets stimulation in oxidative stress underlying diseases. methods: human platelets pretreated with se and stimulated by cu2+-oxidized low density of lipoprotein (oxldl) or thrombin before assessment of p-selectin and phosphorylated p38 mitogen-activated protein kinase (p-p38mapk), phosphorylated jun n-terminal kinase (p– jnk), and phosphorylated extracellular signal-regulated kinases (p-erk1/2). all variables were measured by solid phase sandwich enzyme-linked immunosorbent assay (elisa). results: se significantly decreased cu2+-oxldl induced p-selectin expression, as well as p38 and jnk phosphorylation in platelets, but could not significantly reduce erk1/2 phosphorylation. conclusion: se suppresses inflamed platelets. this effect maybe partly mediated by the p38 or c-jnk signaling pathways. these results create possibility of new co-anti-inflammatory insight for se in atherosclerosis.