Aspirin promotes apoptosis and inhibits proliferation by blocking G0/G1 into S phase in rheumatoid arthritis fibroblast-like synoviocytes via downregulation of JAK/STAT3 and NF-κB signaling pathway

Zhang, X.; Feng, H.; Du, J.; Sun, J.; Li, D.; Hasegawa, T.; Amizuka, N.; Li, Minqi

Aspirin promotes apoptosis and inhibits proliferation by blocking G0/G1 into S phase in rheumatoid arthritis fibroblast-like synoviocytes via downregulation of JAK/STAT3 and NF-κB signaling pathway

Zhang, X.; Feng, H.; Du, J. et al.

International journal of molecular medicine, 2018, 42(6), 3135-3148

Permalink : https://hdl.handle.net/2115/72295

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アクセス権	open access
URI	https://hdl.handle.net/2115/72295
タイトル	Aspirin promotes apoptosis and inhibits proliferation by blocking G0/G1 into S phase in rheumatoid arthritis fibroblast-like synoviocytes via downregulation of JAK/STAT3 and NF-κB signaling pathway
著者	Zhang, X. ; Feng, H. ; Du, J. ; Sun, J. ; Li, D. ; Hasegawa, T. ; Amizuka, N. ; Li, Minqi
著者名 Zhang, X.
著者名 Feng, H.
著者名 Du, J.
著者名 Sun, J.
著者名 Li, D.
e-Rad_Researcher 50739349 著者名 Hasegawa, T.
e-Rad_Researcher 30242431 著者名 Amizuka, N.
e-Rad_Researcher 60447612 著者名 Li, Minqi
言語	英語
キーワード	aspirin
	fibroblast‑like synoviocytes
	apoptosis
	cell cycle
	proliferation
	NF‑κB
	JAK/STAT3
発行日	2018-12
出版者	Spandidos Publications
収録物名	International journal of molecular medicine
巻(号)	42(6)
ページ	3135-3148
抄録	Rheumatoid arthritis (RA) is a commonly occurring autoimmune disease. Its defining pathological characteristic is the excessive proliferation of fibroblast-like synoviocytes (FLS), which is similar to tumor cells and results in a range of clinical problems. As a commonly used antipyretic, analgesic and anti-inflammatory drug, aspirin is the first-line treatment for RA. However, its mechanism of action has not been well explained. The goal is to investigate the biological effects of aspirin on primary RA-FLS and its underlying mechanisms. In this experiment we treated cells with various concentrations of aspirin (0, DMSO, 1, 2, 5, 10 mM). Cell proliferation activity was detected with CCK-8 assays. Apoptosis and cell cycle distribution were detected via flow cytometry. Apoptosis and cell cycle-associated proteins (Bcl-2, Bax, PRAP1, Cyclin D1, P21), as well as the key proteins and their phosphorylation levels of the NF-κB and JAK/STAT3 signaling pathways, were detected via western blot analysis. Bioinformatics prediction revealed that aspirin was closely associated with cell proliferation and apoptosis, including the p53 and NF-κB signaling pathways. By stimulating with aspirin, cell viability decreased, while the proportion of apoptotic cells increased, and the number of cells arrested in the G0/G1 phase increased in a dose-dependent manner. The expression of Bax increased with aspirin stimulation, while the levels of Bcl-2, PRAP1, Cyclin D1 and P21 decreased; p-STAT3, p-P65 and p-50 levels also decreased while STAT3, P65, P50, p-P105 and P105 remained unchanged. From our data, it can be concluded that aspirin is able to promote apoptosis and inhibit the proliferation of RA-FLS through blocking the JAK/STAT3 and NF-κB signaling pathways.
資源タイプ	学術雑誌論文
出版タイプ	Version of Record
PISSN	1107-3756
EISSN	1791-244X
関連情報 (isIdenticalTo)	出版社版DOI https://doi.org/10.3892/ijmm.2018.3883