Sinensetin Inhibits Interleukin-6 in Human Mast Cell - 1 Via Signal Transducers and Activators of the Transcription 3 (STAT3) and Nuclear Factor Kappa B (NF-κB) Pathways
Natural Product Sciences
; : 1-4, 2017.
Article
de En
| WPRIM
| ID: wpr-198630
Bibliothèque responsable:
WPRO
ABSTRACT
Sinensetin, a pentamethoxyflavone, is known to exert various pharmacological activities including anti-angiogenesis, anti-diabetic and anti-inflammatory activities. However, its effects on the human mast cell - 1 (HMC-1) mediated inflammatory mechanism remain unknown. To explore the mediator and cellular inflammatory response of sinensetin, we examined its influence on phorbol 12-myristate 13-acetate (PMA) plus A23187 induced inflammatory mediator production in a human mast cell line. In this study, interleukin (IL)-6 production was measured using the enzyme-linked immunosorbent assay and reverse transcription polymerase chain reaction. Sinensetin inhibited PMA plus A23187 induced IL-6 production in a dose-dependent manner as well as IL-4, IL-5 and IL-8 mRNA expression. Furthermore, sinensetin inhibited signal transducer and activator of transcription 3 (STAT3) phosphorylation, suggesting that sinensetin inhibits the production of inflammatory mediators by blocking STAT3 phosphorylation. Moreover, sinensetin was found to inhibit nuclear factor kappa B activation. These findings suggest that sinensetin may be involved in the regulation of mast cell-mediated inflammatory responses.
Mots clés
Texte intégral:
1
Indice:
WPRIM
Sujet Principal:
Phosphorylation
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Transducteurs
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ARN messager
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Test ELISA
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Réaction de polymérisation en chaîne
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Interleukine-8
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Facteur de transcription NF-kappa B
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A-23187
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Interleukines
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Interleukine-4
Limites du sujet:
Humans
langue:
En
Texte intégral:
Natural Product Sciences
Année:
2017
Type:
Article