TY - JOUR
T1 - Naringenin inhibits dendritic cell maturation and has therapeutic effects in a murine model of collagen-induced arthritis
AU - Li, Yi Rong
AU - Chen, Der Yuan
AU - Chu, Ching Liang
AU - Li, Shiming
AU - Chen, Yu Kuo
AU - Wu, Chao Ling
AU - Lin, Chi Chen
N1 - Publisher Copyright:
© 2015 Elsevier Inc..
PY - 2015/12/1
Y1 - 2015/12/1
N2 - 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.
AB - 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.
UR - http://www.scopus.com/inward/record.url?scp=84983179854&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=84983179854&partnerID=8YFLogxK
U2 - 10.1016/j.jnutbio.2015.07.016
DO - 10.1016/j.jnutbio.2015.07.016
M3 - Article
C2 - 26350255
AN - SCOPUS:84983179854
SN - 0955-2863
VL - 26
SP - 1467
EP - 1478
JO - Journal of Nutritional Biochemistry
JF - Journal of Nutritional Biochemistry
IS - 12
ER -