tbzmedTabriz University of Medical SciencesJCVTRJournal of Cardiovascular and Thoracic ResearchOriginal ArticleJournal of Cardiovascular and Thoracic ResearchEffects of Selenium in the MAPK Signaling CascadeSelenium effect in atherosclerosisRashtchizadeh Nadereh , KarimiPouranTabriz University of Medical Sciences, Neurosciences Research CenterDehganParvin, Salimi MovahedMohamadreza , 9201529201573872015Tabriz University of Medical Sciences2015Effects of Selenium in the MAPK Signaling Cascade

<em><strong>Introduction:</strong></em> This study aimed to discover by which mechanism selenium (Se) suppresses stimulated platelets stimulation in oxidative stress underlying diseases.<br /> <em><strong>Methods:</strong></em> Human platelets pretreated with Se and stimulated by Cu2+-oxidized low density of lipoprotein&nbsp; (OxLDL) or thrombin before assessment of P-selectin and phosphorylated p38 mitogen-activated protein kinase (p-p38MAPK), phosphorylated Jun N-terminal kinase (p&ndash;JNK), and phosphorylated extracellular signal-regulated kinases (p-ERK1/2). All variables were measured by solid phase sandwich enzyme-linked immunosorbent assay (ELISA).<br /> <em><strong>Results: </strong></em>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.<br /> <em><strong>Conclusion:</strong></em> 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.