title: Apigenin inhibits release of inflammatory mediators by blocking the NF-κB activation pathways in the HMC-1 cells.
abstract: Apigenin is a plant flavonoid and a pharmacologically active agent that has been isolated from several plant species. However, the molecular mechanism of apigenin-mediated immune modulation has not been fully understood. One of the possible mechanisms of its protective effects is the down-regulation of inflammatory responses. In this study, we used cells from the human mast cell line (HMC-1) to investigate this effect. Apigenin significantly inhibits the inductive effect of phorbol 12-myristate 13-acetate (PMA) plus A23187 on the production of inflammatory cytokines such as tumor necrosis factor (TNF)-α, interleukin (IL)-8, IL-6, and granulocyte-macrophage colony-stimulating factor (GM-CSF). Moreover, apigenin attenuated the cyclooxygenase (COX)-2 expression and intracellular Ca(2+) level. In activated HMC-1 cells, apigenin inhibited the PMA plus A23187-induced activation of nuclear factor (NF)-κB, IκB degradation, and luciferase activity. Furthermore, apigenin suppressed the expression of TNF-α, IL-8, IL-6, GM-CSF, and COX-2 by decreasing the intracellular Ca(2+) level and inhibiting NF-κB activation. These results indicate that apigenin has a potential regulatory effect on inflammatory reactions that are mediated by mast cells.
authors.affiliation: Department of Oriental Pharmacy, College of Pharmacy, Wonkwang University, Wonkwang Oriental Medicines Research Institute, Iksan, Jeonbuk, Republic of Korea.
authors.forename: Ok-Hwa
authors.initials: OH
authors.lastname: Kang
authors.forename: John-Hwa
authors.initials: JH
authors.lastname: Lee
authors.forename: Dong-Yeul
authors.initials: DY
authors.lastname: Kwon
mesh_terms: D047310:Apigenin / Q000494:pharmacology*; D002118:Calcium / Q000378:metabolism; D002460:Cell Line; D051546:Cyclooxygenase 2 / Q000235:genetics / Q000378:metabolism; D015536:Down-Regulation / Q000235:genetics; D016178:Granulocyte-Macrophage Colony-Stimulating Factor / Q000037:antagonists & inhibitors / Q000097:blood / Q000378:metabolism; D006801:Humans; D007249:Inflammation / Q000188:drug therapy / Q000378:metabolism; D018836:Inflammation Mediators / Q000037:antagonists & inhibitors* / Q000378:metabolism; D015850:Interleukin-6 / Q000378:metabolism; D016209:Interleukin-8 / Q000037:antagonists & inhibitors / Q000378:metabolism; D008156:Luciferases / Q000378:metabolism; D016328:NF-kappa B / Q000037:antagonists & inhibitors* / Q000378:metabolism; D015398:Signal Transduction / Q000187:drug effects; D014409:Tumor Necrosis Factor-alpha / Q000037:antagonists & inhibitors / Q000378:metabolism; D000093242:Interleukin-6 Inhibitors
chemical_list: D047310:Apigenin; D002118:Calcium; D051546:Cyclooxygenase 2; D016178:Granulocyte-Macrophage Colony-Stimulating Factor; D018836:Inflammation Mediators; D015850:Interleukin-6; D016209:Interleukin-8; D008156:Luciferases; D016328:NF-kappa B; D014409:Tumor Necrosis Factor-alpha; D000093242:Interleukin-6 Inhibitors