title: Effects of Selenium in the MAPK Signaling Cascade.
abstract: BACKGROUND
  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 Cu(2+)-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 Cu(2+)-OxLDL induced P-selectin expression, as well as p38 and JNK phosphorylation in platelets, but could not significantly reduce ERK1/2 phosphorylation.
  
  
  CONCLUSIONS
  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.
authors.affiliation: Drug Applied Research Center, Tabriz University of Medical Sciences, Tabriz, Iran.
authors.forename: Nadereh
authors.initials: N
authors.lastname: Rashtchizadeh
authors.affiliation: Neurosciences Research Center, Tabriz University of Medical Sciences, Tabriz, Iran.
authors.forename: Pouran
authors.initials: P
authors.lastname: Karimi
authors.affiliation: Faculty of Nutrition, Tabriz University of Medical Sciences, Tabriz, Iran.
authors.forename: Parvin
authors.initials: P
authors.lastname: Dehgan
authors.affiliation: Faculty of Dentistry, Tabriz University of Medical Sciences, Tabriz, Iran.
authors.forename: Mohamadreza
authors.initials: M
authors.lastname: Salimi Movahed
keywords: Atherosclerosis; Mitogen-Activated Protein Kinase; Platelets; Selenium