| Autor: |
کریمی, پوران, ماکو, روشنک بیات, دهقان, پروین, سلیمی موحد, محمدرضا |
| Zdroj: |
Arak Medical University Journal; 2014, Vol. 17 Issue 1, p63-75, 13p |
| Abstrakt: |
Background: Selenium is a unique trace element which is beneficial on inflammatory underlining diseases. Mitogen-Activated Protein Kinase (MAPK) pathways regulate several cellular functions including inflammation, cell differentiation, migration, and apoptosis. This study aimed to find out the pathway(s) by which Selenium modifies inflammatory events in oxidative or thrombotic induced stress in platelets. Material 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-Jun N-terminal Kinase (c-JNK), and Extracellular Signal-Regulated Kinases1/2(ERK1/2) 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-Immuno Sorbent Assay). Pharmacological inhibition was 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 could not significantly reduce thrombin induced P-selectin despite of decreasing in mentioned phospho-proteins. 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. [ABSTRACT FROM AUTHOR] |
| Databáze: |
Complementary Index |
| Externí odkaz: |
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