Inhibitory effect of kaempferol on inflammatory response of lipopolysaccharide-stimulated human mast cells.
- Author:
Yun-jiang ZHOU
;
Hu WANG
;
Li LI
;
He-huan SUI
;
Jia-jun HUANG
- Publication Type:Journal Article
- MeSH:
Cells, Cultured;
Histamine;
metabolism;
Humans;
I-kappa B Kinase;
metabolism;
I-kappa B Proteins;
metabolism;
Inflammation;
metabolism;
Interleukin-1beta;
metabolism;
Interleukin-6;
metabolism;
Interleukin-8;
metabolism;
Kaempferols;
pharmacology;
Lipopolysaccharides;
Mast Cells;
drug effects;
NF-KappaB Inhibitor alpha;
NF-kappa B;
metabolism;
Tumor Necrosis Factor-alpha;
metabolism
- From:
Acta Pharmaceutica Sinica
2015;50(6):702-707
- CountryChina
- Language:Chinese
-
Abstract:
This study is to investigate the inhibitory effect of kaempferol on inflammatory response of lipopolysaccharide(LPS)-stimulated HMC-1 mast cells. The cytotoxicity of kaempferol to HMC-1 mast cells were analyzed by using MTT assay and then the administration concentrations of kaempferol were established. Histamine, IL-6, IL-8, IL-1β and TNF-α were measured using ELISA assay in activated HMC-1 mast cells after incubation with various concentrations of kaempferol (10, 20 and 40 µmol.L-1). Western blot was used to test the protein expression of p-IKKβ, IκBα, p-IκBα and nucleus NF-κB of LPS-induced HMC-1 mast cells after incubation with different concentrations of kaempferol. The optimal concentrations of kaempferol were defined as the range from 5 µmol.L-1 to 40 µmol.L-1. Kaempferol significantly decreased the release of histamine, IL-6, IL-8, IL-1β and TNF-α of activated HMC-1 mast cells (P<0.01). After incubation with kaempferol, the protein expression of p-IKKβ, p-IKBa and nucleus NF-κB (p65) markedly reduced in LPS-stimulated HMC-1 mast cells (P<0.01). Taken together, we concluded that kaempferol markedly inhibit mast cell-mediated inflammatory response. At the same time, kaempferol can inhibit the activation of IKKβ, block the phosphorylation of IκBα, prevent NF-KB entering into the nucleus, and then decrease the release of inflammatory mediators.
