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.
- Author:
Hee Sung CHAE
1
;
Young Mi KIM
;
Young Won CHIN
Author Information
- Publication Type:Original Article
- Keywords: Sinensetin; Interleukin-6; STAT3; NF-κB
- MeSH: Calcimycin; Enzyme-Linked Immunosorbent Assay; Humans*; Interleukin-4; Interleukin-5; Interleukin-6*; Interleukin-8; Interleukins; Mast Cells*; NF-kappa B*; Phosphorylation; Polymerase Chain Reaction; Reverse Transcription; RNA, Messenger; STAT3 Transcription Factor; Transducers*
- From:Natural Product Sciences 2017;23(1):1-4
- CountryRepublic of Korea
- Language:English
- 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.
