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10.15171/jcvtr.2015.23 http://scihub22266oqcxt.onion/10.15171/jcvtr.2015.23 C4586596!4586596!26430498     free     free     free       J+Cardiovasc+Thorac+Res 2015 ; 7 (3): 107-12 Nephropedia Template TP {{tp|p=26430498|t=2015. Effects of Selenium in the MAPK Signaling Cascade |pdf=|usr=}}{{26430498}} gab.com Text Effects of Selenium in the MAPK Signaling Cascade JO: J Cardiovasc Thorac Res http://www.kidney.de/pget.php?&tw=1&pmid=26430498 #FOAvip 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. Twit Text FOAVip Effects of Selenium in the MAPK Signaling Cascade ????J Cardiovasc Thorac Res http://www.kidney.de/pget.php?&tw=1&pmid=26430498 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=26430498 #FOAvip English Wikipedia <ref>{{Cite pmid|26430498}}</ref> Effects of Selenium in the MAPK Signaling Cascade #MMPMID26430498 Rashtchizadeh N; Karimi P; Dehgan P; Salimi Movahed M J Cardiovasc Thorac Res 2015[]; 7 (3): 107-12 PMID26430498show ga 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. äEffects of Selenium in the MAPK Signaling Cascade (epmc).pdf DeepDyve Pubget Overpricing