Volume 17, Issue 1 (4-2014)                   J Arak Uni Med Sci 2014, 17(1): 0-0 | Back to browse issues page

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Karimi P, Bayat Makou R, Dehghan P, Salimi Movahed M R. Selenium Relieves Inflamation in Oxidized- LDL Activated Platelets via P38MAPK Pathway. J Arak Uni Med Sci 2014; 17 (1)
URL: http://jams.arakmu.ac.ir/article-1-2566-en.html
1- Department of biochemistry, School of Medicine, Tabriz University of Medical Sciences, Tabriz, Iran , pouran.karimi@yahoo.com
2- Faculty of Medicine, Islamic Azad University Tabriz Medical Sciences Branch, Tabriz, Iran
3- Faculty of Nutrition, Tabriz University of Medical Sciences, Tabriz, Iran
4- Student of Dentistry, International Branch of Tabriz University of Medical Sciences, Tabriz, Iran
Abstract:   (10458 Views)

 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.

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Type of Study: Original Atricle | Subject: Basic Sciences
Received: 2013/10/11 | Accepted: 2014/02/26

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