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Effects of Selenium in the MAPK Signaling Cascade.


ABSTRACT: 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 Cu(2+)-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 Cu(2+)-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.

SUBMITTER: Rashtchizadeh N 

PROVIDER: S-EPMC4586596 | biostudies-other | 2015

REPOSITORIES: biostudies-other

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Effects of Selenium in the MAPK Signaling Cascade.

Rashtchizadeh Nadereh N   Karimi Pouran P   Dehgan Parvin P   Salimi Movahed Mohamadreza M  

Journal of cardiovascular and thoracic research 20150101 3


<h4>Introduction</h4>This study aimed to discover by which mechanism selenium (Se) suppresses stimulated platelets stimulation in oxidative stress underlying diseases.<h4>Methods</h4>Human platelets pretreated with Se and stimulated by Cu(2+)-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 kin  ...[more]

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