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Effects of Selenium in the MAPK Signaling Cascade
Nadereh Rashtchizadeh1, Pouran Karimi2, Parvin Dehgan3
1Drug Applied Research Center, Tabriz University of Medical Sciences, Tabriz, Iran.
Journal of Cardiovascular and Thoracic Research
|October 3, 2015
Summary
Selenium (Se) suppresses platelet inflammation by inhibiting p38 and JNK pathways, offering potential co-anti-inflammatory benefits in atherosclerosis. This study reveals a key mechanism for Se
Area of Science:
- Biochemistry
- Immunology
- Cardiovascular Research
Background:
- Oxidative stress exacerbates platelet stimulation in various diseases.
- Platelet activation plays a critical role in inflammatory processes.
Purpose of the Study:
- To elucidate the mechanism by which selenium (Se) suppresses platelet activation under oxidative stress conditions.
- To investigate the role of specific signaling pathways in Se-mediated platelet suppression.
Main Methods:
- Human platelets were pretreated with selenium (Se).
- Platelets were stimulated with Cu(2+)-oxidized low-density lipoprotein (OxLDL) or thrombin.
- P-selectin expression and phosphorylation of p38 MAPK, JNK, and ERK1/2 were measured using ELISA.
Main Results:
- Selenium significantly reduced Cu(2+)-OxLDL-induced P-selectin expression.
- Se treatment significantly inhibited the phosphorylation of p38 MAPK and JNK.
- No significant effect of Se was observed on ERK1/2 phosphorylation.
Conclusions:
- Selenium effectively suppresses platelet inflammation.
- The anti-inflammatory effect of Se on platelets may involve the p38 and c-JNK signaling pathways.
- These findings suggest a potential role for Se as a co-anti-inflammatory agent in atherosclerosis.
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