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

Authors :
Seung Woong Lee
So Nam Kim
Hyun-Mee Oh
Byung Soon Hwang
Bo Ra Yun
Chan Sun Park
See-Hwa Jeoung
Woo Song Lee
Hyun-Kyu Kim
Mun-Chual Rho
Source :
Rheumatology. 53:56-64
Publication Year :
2013
Publisher :
Oxford University Press (OUP), 2013.

Abstract

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 collagen-induced 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 inflammation-related 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.

Details

ISSN :
14620332 and 14620324
Volume :
53
Database :
OpenAIRE
Journal :
Rheumatology
Accession number :
edsair.doi.dedup.....f25fd361152de50bb76749f94acd5a05
Full Text :
https://doi.org/10.1093/rheumatology/ket302