|Title:||Naringenin inhibits dendritic cell maturation and has therapeutic effects in a murine model of collagen-induced arthritis||Authors:||Li, Yi-Rong
|Keywords:||Collagen-induced arthritis; Dendritic cells; Flavonoid; Maturation; Naringenin||Issue Date:||2015||Source:||Journal of Nutritional Biochemistry||Abstract:||
The aim of this study was to investigate the effect of naringenin (5,7,4'-trihydroxyflavanone), a citrus flavonoid, on dendritic cell (DC) maturation, as well as its potential as a therapeutic agent in a murine model of collagen-induced arthritis (CIA). Naringenin effectively inhibited lipopolysaccharide (LPS)-induced DC maturation as shown by reductions in the production of proinflammatory cytokines/chemokines, the expression of costimulatory molecules and the Ag-specific T cell priming ability of DCs when given at noncytotoxic doses. In addition, the decrease of LPS-induced MAPK and NF-κB signaling activation may contribute to the inhibitory activity of naringenin. In mice with CIA, the oral administration of naringenin ameliorated the severity of arthritis, reduced the levels of anticollagen Type II (CII) IgG and limited the proliferation of T cells, observed as a lower frequency of Th1 and Th17 cells in the spleen after restimulation with CII. In conclusion, this study shows for the first time that naringenin can manipulate the immunostimulatory properties of DCs and thus represents a potential therapeutic for the treatment of rheumatoid arthritis in humans. ? 2015 Elsevier Inc..
|DOI:||10.1016/j.jnutbio.2015.07.016||SDG/Keyword:||chemokine; collagen type 2; cytokine; immunoglobulin enhancer binding protein; immunoglobulin G; lipopolysaccharide; mitogen activated protein kinase; naringenin; collagen; flavanone derivative; immunoglobulin enhancer binding protein; immunoglobulin G; ligand; naringenin; adult; animal experiment; animal model; animal tissue; arthritis; Article; cell contact; cell maturation; controlled study; cytokine production; dendritic cell; disease severity; dose response; drug effect; drug mechanism; immunostimulation; lymphocyte proliferation; male; mouse; nonhuman; protein expression; signal transduction; spleen; stent; T lymphocyte; T lymphocyte activation; Th1 cell; Th17 cell; animal; blood; C57BL mouse; CD4+ T lymphocyte; cell proliferation; cell survival; chemistry; cytology; dendritic cell; disease model; experimental arthritis; inflammation; metabolism; oral drug administration; rheumatoid arthritis; transgenic mouse; Administration, Oral; Animals; Arthritis, Experimental; Arthritis, Rheumatoid; CD4-Positive T-Lymphocytes; Cell Proliferation; Cell Survival; Collagen; Dendritic Cells; Disease Models, Animal; Dose-Response Relationship, Drug; Flavanones; Immunoglobulin G; Inflammation; Ligands; Lipopolysaccharides; Male; Mice; Mice, Inbred C57BL; Mice, Transgenic; NF-kappa B; Signal Transduction; Spleen; Th1 Cells; Th17 Cells
|Appears in Collections:||免疫學研究所|
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