Lobaric Acid Inhibits VCAM-1 Expression in TNF-alpha-Stimulated Vascular Smooth Muscle Cells via Modulation of NF-kappaB and MAPK Signaling Pathways.
10.4062/biomolther.2015.084
- Author:
Ii Seul KWON
1
;
Joung Han YIM
;
Hong Kum LEE
;
Suhkneung PYO
Author Information
1. School of Pharmacy, Sungkyunkwan University, Suwon 16419, Republic of Korea. snpyo@skku.edu
- Publication Type:Original Article
- Keywords:
Lobaric acid;
Atherosclerosis;
VCAM-1;
MAPK;
NF-kappaB;
MOVAS-1
- MeSH:
Animals;
Atherosclerosis;
Blotting, Western;
Down-Regulation;
Enzyme-Linked Immunosorbent Assay;
Extracellular Signal-Regulated MAP Kinases;
Inflammation;
Lichens;
Mice;
Muscle, Smooth, Vascular*;
NF-kappa B*;
Phosphorylation;
Phosphotransferases;
Physiology;
Tumor Necrosis Factor-alpha;
Vascular Cell Adhesion Molecule-1*
- From:Biomolecules & Therapeutics
2016;24(1):25-32
- CountryRepublic of Korea
- Language:English
-
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.
