Vigna angularis inhibits IL-6-induced cellular signalling and ameliorates collagen-induced arthritis.
Rheumatology (Oxford)
; 53(1): 56-64, 2014 Jan.
Article
en En
| MEDLINE
| ID: mdl-24097134
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.
Palabras clave
Texto completo:
1
Colección:
01-internacional
Banco de datos:
MEDLINE
Asunto principal:
Artritis Experimental
/
ARN
/
Extractos Vegetales
/
Regulación de la Expresión Génica
/
Interleucina-6
/
Factor de Transcripción STAT3
Límite:
Animals
/
Humans
/
Male
Idioma:
En
Revista:
Rheumatology (Oxford)
Asunto de la revista:
REUMATOLOGIA
Año:
2014
Tipo del documento:
Article