Ok-Hwa Kang, Nam-Won Kwak, Yun-Soo Seo, Tian Zhou, Ryong Kong, Sang-A Kim, Dong-Won Shin, Dong-Yeul Kwon
Objective: Curcumin [1,7-bis-(4-hydroxy-3-methoxyphenyl-1,6-hepatadiene-3,5-dione], the active component of turmeric, is a polyphenolic phytochemical with anti-tumor, anti-inflammatory, anti-oxidative, and anti-allergic properties. To ascertain the molecular mechanism involved in the anti-inflammatory activity of Curcumin, phorbol-12-myristate-13-acetate (PMA) plus A23187 treatment was used to induce inflammation in human mast cell line 1 (HMC-1). Methods: HMC-1 cells were pre-treated with Curcumin prior to stimulation with PMA plus A23187. Curcumin inhibited the induction of inflammatory cytokines such as interleukin (IL)-6, IL-8, and tumor necrosis factor (TNF)-α caused by treatment with PMA plus A23187. Results: Curcumin attenuated the expression of cyclooxygenase (COX)-2. In activated HMC-1 cells, phosphorylation levels of extra-signal response kinase (ERK) and p38 mitogen-activated protein kinase, but not c-jun N-terminal Kinase (JNK), were decreased by treatment with Curcumin. Curcumin also inhibited nuclear factor (NF)-κB activation, IκB degradation, and phosphorylation induced by PMA plus A23187. Conclusion: Curcumin suppressed expression of TNF-α, IL-8, IL-6, and COX-2 through blocking NF-κB and MAP kinase signalling pathways.