Kaempferol inhibits IL‑1β‑induced proliferation of rheumatoid arthritis synovial fibroblasts and the production of COX‑2, PGE2 and MMPs
- Authors
- Yoon, Ha-Yong; Lee, Eun-Gyeong; Lee, Hyun; Cho, In Jin; Choi, Yun Jung; Sung, Myung-Soon; Yoo, Han-Gyul; Yoo, Wan-Hee
- Issue Date
- Oct-2013
- Publisher
- SPANDIDOS PUBL LTD
- Keywords
- cyclooxygenase; interleukin-1 beta; prostaglandin E2; matrix metalloproteinases; rheumatoid arthritis; kaempferol
- Citation
- INTERNATIONAL JOURNAL OF MOLECULAR MEDICINE, v.32, no.4, pp.971 - 977
- Indexed
- SCIE
SCOPUS
- Journal Title
- INTERNATIONAL JOURNAL OF MOLECULAR MEDICINE
- Volume
- 32
- Number
- 4
- Start Page
- 971
- End Page
- 977
- URI
- https://scholarworks.bwise.kr/hanyang/handle/2021.sw.hanyang/161708
- DOI
- 10.3892/ijmm.2013.1468
- ISSN
- 1107-3756
- Abstract
- Inflammatory cytokines, matrix metalloproteinases (MMPs) and cyclooxygenase (COX)-2 released from rheumatoid arthritis synovial fibroblasts (RASFs) are involved in the destruction of both articular bone and cartilage. Kaempferol has been reported to act as an antioxidant and anti-inflammatory agent by inhibiting nitric oxide synthase and COX enzymes. The aim of the present study was to determine the effects of kaempferol on the interleukin-1 beta (IL-1 beta)-induced proliferation of RASFs and the production of MMPs, COX and prostaglandin E2 (PGE2) by RASFs. The proliferation of the RASFs stimulated with IL-1 beta and treated with/without kaempferol was evaluated by CCK-8 assay. The expression of MMPs, TIMP metallopeptidase inhibitor-1 (TIMP-1), COXs, PGE2 and that of intracellular MAPK signaling molecules, including p-ERK, p-p38, p-JNK and nuclear factor-kappa B (NF-kappa B) was examined by immunoblotting or semi-quantitative reverse transcription-polymerase chain reaction (RT-PCR) and ELISA under the conditions described above. Kaempferol inhibited the proliferation of both unstimulated and IL-1 beta-stimulated RASFs, as well as the mRNA and protein expression of MMP-1, MMP-3, COX-2 and PGE2 induced by IL-1 beta. Kaempferol also inhibited the phosphorylation of ERK-1/2, p38 and JNK, as well as the activation of NF-kappa B induced by IL-1 beta. These results indicate that kaempferol inhibits synovial fibroblast proliferation, as well as the production of and MMPs, COX-2 and PGE2, which is involved in articular inflammation and destruction in rheumatoid arthritis (RA). Our data suggest that kaempferol may be a novel therapeutic agent for the treatment of RA.
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