Vigna angularis inhibits IL-6-induced cellular signalling and ameliorates collagen-induced arthritis

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Vigna angularis inhibits IL-6-induced cellular signalling and ameliorates collagen-induced arthritis
Hyun-Mee Oh; Seung Woong Lee; B R Yun; B S Hwang; S N Kim; Chan Sun Park; S H Jeoung; H K Kim; Woo Song LeeMun Chual Rho
Bibliographic Citation
Rheumatology, vol. 53, no. 1, pp. 56-64
Publication Year
Objectives: The present study was conducted in order to assess whether extracts or isolated compounds from Vigna angularis were able to suppress IL-6 signalling and to show the therapeutic effect on collageninduced arthritis (CIA) in mice. Methods: The effect of V. angularis on IL-6 signalling was studied by measuring Stat3-dependent luciferase activity, expression of inflammation-related genes, and phosphorylation of Janus kinase 2 (JAK2), signal transducer and activator of transcription 3 (STAT3) and extracellular signal-regulated kinase (ERK) induced by IL-6. CIA was induced by immunizing with bovine type II collagen. V. angularis extract (VAE) was administrated orally at 50 and 100 mg/kg from day 1 to day 28. Induction of arthritis was evaluated with a visual scoring system and histological analysis. Results: Extracts or two triterpenoid compounds from V. angularis showed potent inhibitory effects on pSTAT3-inducible luciferase activity, STAT3 tyrosine phosphorylation and the expression of inflammationrelated genes induced by IL-6. Administration of VAE significantly suppressed the progression of CIA, accompanied by a reduced antibody response to type II collagen and protection from tissue damage in knee joints. Conclusion: Administration of VAE has a therapeutic effect on CIA and this effect is associated with the inhibitory activity on IL-6/STAT3 signalling. These results suggest that extracts or compounds from V. angularis could be a useful treatment for diseases related to IL-6, including RA.
Collagen-induced arthritisIL-6Rheumatoid arthritisSTAT3Vigna angularis
Oxford Univ Press
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Jeonbuk Branch Institute > Functional Biomaterial Research Center > 1. Journal Articles
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