Background: Selenium is a unique trace element which is benefit on inflammatory underlining diseases. MAPK (Mitogen-activated protein kinase) pathways regulate several cellular functions including inflammation, cell differentiation, migration, and apoptosis. Objective: This study aimed to find out the pathway(s) by which Selenium modifies inflammatory events in oxidative or thrombotic induced stress in platelet.

Materials and Methods: This is a basic -experimental study on Human platelets obtained from 30 healthy individuals (age 35±12) .The phosphorylation rate of P38MAPK , c –JNK (c-Jun N-terminal Kinase), and ERK1/2(Extracellular signal-regulated kinases1/2) as three important proteins in MAPK family and P-selectin were measured in presence or absence of selenium by ELISA( solid phase sandwich Enzyme Linked-ImmunoSorbent Assay). Pharmacological inhibition is done by inhibitors of P38MAPK, ERK1/2 and c- JNK in order to compare with selenium effects. The percentage of ratio of phosphorylated to total protein was used for normalizing the phospho protein contents of platelets.

Results: Selenium significantly reduced P-selectin expression (p<0.05), P38MAPK (p<0.05) and c- JNK phosphorylation (p<0.05) induced by cu2+oxidized LDL in platelets but Se couldn’t significantly reduce Thrombin induced P-selectin despite of decreasing in mentioned phospho-proeins.

Conclusion: Our results indicated that Selenium can reduce inflammation via suppression of p38MAPK-dependent signaling pathway. These results may provide insights related to development of novel Selenium therapies in atherosclerosis.