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Kaempferitrin inhibits proliferation, induces apoptosis, and ameliorates inflammation in human rheumatoid arthritis fibroblast‐like synoviocytes
Author(s) -
Wang Jing,
Zhao Qing
Publication year - 2019
Publication title -
phytotherapy research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.019
H-Index - 129
eISSN - 1099-1573
pISSN - 0951-418X
DOI - 10.1002/ptr.6364
Subject(s) - pi3k/akt/mtor pathway , inflammation , protein kinase b , apoptosis , tumor necrosis factor alpha , matrix metalloproteinase , fibroblast , cancer research , rheumatoid arthritis , chemistry , arthritis , interleukin 6 , signal transduction , cell growth , proinflammatory cytokine , interleukin , cytokine , pharmacology , immunology , medicine , biochemistry , in vitro
Rheumatoid arthritis (RA) is a complex chronic inflammatory disease that is associated with the aberrant activation of fibroblast‐like synoviocytes (FLS). Kaempferitrin is a natural flavonoid glycoside that possesses anti‐inflammatory bioactivity. However, the effect of kaempferitrin on RA has not yet been revealed. The aim of the present study was to investigate the effect of kaempferitrin on human RA‐FLS MH7A cell line. We found that kaempferitrin inhibited proliferation and induced apoptosis of MH7A cells. Kaempferitrin decreased the levels of interleukin (IL)‐1β, IL‐6, tumor necrosis factor (TNF)‐α, matrix metalloproteinase (MMP)‐1, and MMP‐3 in MH7A cells. Moreover, kaempferitrin blocked the activation of nuclear factor‐κB (NF‐κB) and protein kinase B (Akt)/mammalian target of rapamycin (mTOR) pathways. Furthermore, treatment with kaempferitrin decreased paw thickness and arthritis scores, and reduced the serum levels of IL‐1β, IL‐6, and TNF‐α in a collagen‐induced arthritis mouse model. In conclusion, kaempferitrin inhibited cell proliferation, induced cell apoptosis, and ameliorated inflammation of RA‐FLS by suppressing the NF‐κB and Akt/mTOR pathways.