Premium
Eriodictyol inhibits survival and inflammatory responses and promotes apoptosis in rheumatoid arthritis fibroblast‐like synoviocytes through AKT/FOXO1 signaling
Author(s) -
Liu YingChun,
Yan XiaoNing
Publication year - 2019
Publication title -
journal of cellular biochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.028
H-Index - 165
eISSN - 1097-4644
pISSN - 0730-2312
DOI - 10.1002/jcb.28724
Subject(s) - eriodictyol , foxo1 , protein kinase b , apoptosis , inflammation , cancer research , pi3k/akt/mtor pathway , tumor necrosis factor alpha , signal transduction , arthritis , rheumatoid arthritis , medicine , immunology , chemistry , pharmacology , luteolin , flavonoid , biochemistry , antioxidant
2‐(3,4‐Dihydroxyphenyl)‐5,7‐dihydroxy‐2,3‐dihydrochromen‐4‐one (eriodictyol), a flavonoid compound, was proved to possess anti‐inflammatory, antioxidative, and antiarthritis activities. However, the effects of eriodictyol on the rheumatoid proliferation, apoptosis, and inflammatory response of arthritis fibroblast‐like synoviocytes (RA‐FLS) remain unclear. Thus, the objective of this study was to examine the effects of eriodictyol on RA‐FLS survival, apoptosis, and inflammatory response, and further explore the potential underlying mechanisms. Our results showed that eriodictyol inhibited the survival of RA‐FLSs and promoted its apoptosis. Eriodictyol significantly reduced RA‐FLS secretion of tumor necrosis factor α, interleukin 6 (IL‐6), IL‐8, and IL‐1β. Furthermore, eriodictyol prevented the activation of the protein kinase B (AKT) pathway and increased the expression of forkhead box O1 (FOXO1) in RA‐FLS. FOXO1 silence reversed the effects of eriodictyol on RA‐FLS survival, apoptosis, and inflammation. In conclusion, these findings indicated that eriodictyol inhibits the cell survival and inflammatory response in RA‐FLS, and the AKT/FOXO1 signaling pathway is involved in the effect of eriodictyol on the RA‐FLS. Thus, eriodictyol might be a potential therapeutic agent for the treatment of rheumatoid arthritis.