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Effects of Caffeoylquinic Acid Derivative Fractions in Miao Medicine Periploca forrestii on Proliferation and Secretion of Inflammatory Cytokines in Human Rheumatoid Arthritis Fibroblast-like Synoviocytes MH7A / 中国药房
China Pharmacy ; (12): 3949-3952, 2017.
Article en Zh | WPRIM | ID: wpr-662033
Biblioteca responsable: WPRO
ABSTRACT
OBJECTIVE:To study the effects of caffeoylquinic acid derivative fractions (CADF) in Miao medicine Periploca forrestii on proliferation and secretion of inflammatory cytokines in tumor necrosis factor α(TNF-α)-induced human rheumatoid ar-thritis(RA)fibroblast-like synoviocytes MH7A,and explore its mechanism on anti-RA. METHODS:MH7A cells were divided in-to blank group,TNF-α model group,methotrexate group (positive control,20 mg/L) and CADF different mass concentrations groups(50,100,200,400 mg/L). Except for blank group,other groups received 50 μg/L of TNF-α to stimulate MH7A cells. Af-ter treated by suspension with TNF-α and related medicines for 24 h,the cell proliferation and contents of nitric oxide(NO),pros-taglandin E2 (PGE2),interleukin 1β(IL-1β),interleukin 6 (IL-6) in culture medium were detected. RESULTS:Compared with blank group,cell proliferation activity in TNF-αmodel group was significantly enhanced(P<0.01),contents of NO,PGE2,IL-1β, IL-6 in culture medium were significantly increased(P<0.01). Compared with TNF-α model group,cell proliferation in each ad-ministration group were significantly inhibited(P<0.05 or P<0.01),contents of NO,PGE2,IL-1β,IL-6 in culture medium weresignificantly decreased (P<0.01),showing certain dose-effect relationship with CADF. CONCLUSIONS:CADF can play the role in anti-RA by inhibiting the TNF-α-induced prolifera-tion of MH7A cells and reducing the secretion of inflammatory cytokines NO,PGE2,IL-1β,IL-6.
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Texto completo: 1 Índice: WPRIM Tipo de estudio: Prognostic_studies Idioma: Zh Revista: China Pharmacy Año: 2017 Tipo del documento: Article
Texto completo: 1 Índice: WPRIM Tipo de estudio: Prognostic_studies Idioma: Zh Revista: China Pharmacy Año: 2017 Tipo del documento: Article