KMID : 0606920160240010025
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Biomolecules & Therapeutics 2016 Volume.24 No. 1 p.25 ~ p.32
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Lobaric Acid Inhibits VCAM-1 Expression in TNF-¥á-Stimulated Vascular Smooth Muscle Cells via Modulation of NF-¥êB and MAPK Signaling Pathways
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Kwon Ii-Seul
Yim Joung-Han Lee Hong-Kum Pyo Suhk-Neung
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Abstract
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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-¥á)-stimulated mouse vascular smooth muscle cells. Western blot and ELISA showed that the increased expression of VCAM-1 by TNF-¥á was significantly suppressed by the pre-treatment of lobaric acid (0.1?10 ¥ìg/ml) for 2 h. Lobaric acid abrogated TNF-¥á-induced NF-¥êB activity through preventing the degradation of I¥êB 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-¥á receptor 1 (TNF-R1). Overall, our results suggest that lobaric acid inhibited VCAM-1 expression through the inhibition of p38, ERK, JNK and NF-¥êB 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.
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KEYWORD
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Lobaric acid, Atherosclerosis, VCAM-1, MAPK, NF-¥êB, MOVAS-1
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