Effects of Selenium in the MAPK Signaling Cascade
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 assessme...
| Main Authors: | , , , |
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| Format: | Article |
| Language: | English |
| Published: |
Tabriz University of Medical Sciences
2015-09-01
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| Series: | Journal of Cardiovascular and Thoracic Research |
| Subjects: | |
| Online Access: | http://journals.tbzmed.ac.ir/JCVTR/PDF/JCVTR-7-107.pdf |
| Summary: | 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. |
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| ISSN: | 2008-5117 2008-6830 |