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...
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Tabriz University of Medical Sciences
2015-09-01
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Online Access: | http://journals.tbzmed.ac.ir/JCVTR/PDF/JCVTR-7-107.pdf |
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doaj-513d39dc69a14055bd081f31b80ccf0e2020-11-24T23:58:38ZengTabriz University of Medical SciencesJournal of Cardiovascular and Thoracic Research2008-51172008-68302015-09-017310711210.15171/jcvtr.2015.23JCVTR_2224_20140914105222Effects of Selenium in the MAPK Signaling CascadeNadereh Rashtchizadeh0Pouran KarimiParvin Dehgan1Mohamadreza Salimi Movahed2Drug Applied Research Center, Tabriz University of Medical Sciences, Tabriz, IranFaculty of Nutrition, Tabriz University of Medical Sciences, Tabriz, IranFaculty of Dentistry, Tabriz University of Medical Sciences, Tabriz, IranIntroduction: 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.http://journals.tbzmed.ac.ir/JCVTR/PDF/JCVTR-7-107.pdfAtherosclerosisMitogen-Activated Protein kinasePlateletsSelenium |
collection |
DOAJ |
language |
English |
format |
Article |
sources |
DOAJ |
author |
Nadereh Rashtchizadeh Pouran Karimi Parvin Dehgan Mohamadreza Salimi Movahed |
spellingShingle |
Nadereh Rashtchizadeh Pouran Karimi Parvin Dehgan Mohamadreza Salimi Movahed Effects of Selenium in the MAPK Signaling Cascade Journal of Cardiovascular and Thoracic Research Atherosclerosis Mitogen-Activated Protein kinase Platelets Selenium |
author_facet |
Nadereh Rashtchizadeh Pouran Karimi Parvin Dehgan Mohamadreza Salimi Movahed |
author_sort |
Nadereh Rashtchizadeh |
title |
Effects of Selenium in the MAPK Signaling Cascade |
title_short |
Effects of Selenium in the MAPK Signaling Cascade |
title_full |
Effects of Selenium in the MAPK Signaling Cascade |
title_fullStr |
Effects of Selenium in the MAPK Signaling Cascade |
title_full_unstemmed |
Effects of Selenium in the MAPK Signaling Cascade |
title_sort |
effects of selenium in the mapk signaling cascade |
publisher |
Tabriz University of Medical Sciences |
series |
Journal of Cardiovascular and Thoracic Research |
issn |
2008-5117 2008-6830 |
publishDate |
2015-09-01 |
description |
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. |
topic |
Atherosclerosis Mitogen-Activated Protein kinase Platelets Selenium |
url |
http://journals.tbzmed.ac.ir/JCVTR/PDF/JCVTR-7-107.pdf |
work_keys_str_mv |
AT naderehrashtchizadeh effectsofseleniuminthemapksignalingcascade AT pourankarimi effectsofseleniuminthemapksignalingcascade AT parvindehgan effectsofseleniuminthemapksignalingcascade AT mohamadrezasalimimovahed effectsofseleniuminthemapksignalingcascade |
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