Lobaric Acid Inhibits VCAM-1 Expression in TNF-alpha-Stimulated Vascular Smooth Muscle Cells via Modulation of NF-kappaB and MAPK Signaling Pathways
Biomolecules & Therapeutics
;
: 25-32, 2016.
Article
Dans Anglais
| WPRIM
| ID: wpr-20742
ABSTRACT
Lichens have been known to possess multiple biological activities, including anti-proliferative and anti-inflammatory activities. Vascular cell adhesion molecule-1 (VCAM-1) may play a role in the development of atherosclerosis. Hence, VCAM-1 is a possible therapeutic target in the treatment of the inflammatory disease. However, the effect of lobaric acid on VCAM-1 has not yet been investigated and characterized. For this study, we examined the effect of lobaric acid on the inhibition of VCAM-1 in tumor necrosis factor-alpha (TNF-alpha)-stimulated mouse vascular smooth muscle cells. Western blot and ELISA showed that the increased expression of VCAM-1 by TNF-alpha was significantly suppressed by the pre-treatment of lobaric acid (0.1-10 mug/ml) for 2 h. Lobaric acid abrogated TNF-alpha-induced NF-kappaB activity through preventing the degradation of IkappaB and phosphorylation of extracellular signal-regulated kinases (ERK), c-Jun N-terminal kinases (JNK), and p38 mitogen activated protein (MAP) kinase. Lobaric acid also inhibited the expression of TNF-alpha receptor 1 (TNF-R1). Overall, our results suggest that lobaric acid inhibited VCAM-1 expression through the inhibition of p38, ERK, JNK and NF-kappaB signaling pathways, and downregulation of TNF-R1 expression. Therefore, it is implicated that lobaric acid may suppress inflammation by altering the physiology of the atherosclerotic lesion.
Texte intégral:
Disponible
Indice:
WPRIM (Pacifique occidental)
Sujet Principal:
Phosphorylation
/
Phosphotransferases
/
Physiologie
/
Test ELISA
/
Régulation négative
/
Technique de Western
/
Facteur de transcription NF-kappa B
/
Facteur de nécrose tumorale alpha
/
Molécule-1 d'adhérence des cellules vasculaires
/
Extracellular Signal-Regulated MAP Kinases
Limites du sujet:
Animaux
langue:
Anglais
Texte intégral:
Biomolecules & Therapeutics
Année:
2016
Type:
Article
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