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KMID : 0620720170230010001
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Natural Product Sciences
2017 Volume.23 No. 1 p.1 ~ p.4
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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
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Chae Hee-Sung
Kim Young-Mi
Chin Young-Won
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Abstract
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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.
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KEYWORD
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Sinensetin, Interleukin-6, STAT3, NF-κB
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