{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,6,8]],"date-time":"2026-06-08T10:07:13Z","timestamp":1780913233023,"version":"3.54.1"},"reference-count":31,"publisher":"Wiley","issue":"1","license":[{"start":{"date-parts":[[2026,6,8]],"date-time":"2026-06-08T00:00:00Z","timestamp":1780876800000},"content-version":"vor","delay-in-days":158,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"},{"start":{"date-parts":[[2026,1,1]],"date-time":"2026-01-01T00:00:00Z","timestamp":1767225600000},"content-version":"tdm","delay-in-days":0,"URL":"http:\/\/doi.wiley.com\/10.1002\/tdm_license_1.1"}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Mediators of Inflammation"],"published-print":{"date-parts":[[2026,1]]},"abstract":"<jats:sec>\n                    <jats:title>Objective<\/jats:title>\n                    <jats:p>The objective of this study was to investigate whether hydroxysafflor yellow A (HSYA) affects the proliferation and apoptosis of fibroblast\u2010like synoviocytes (FLSs) in rheumatoid arthritis (RA). Synovial fibroblast hyperplasia is a key pathological feature of RA, and its inhibition may slow disease progression. Although HSYA has attracted significant interest, its effects on RA are not yet fully understood. Thus, we performed a series of experiments to examine the impact of HSYA on FLSs.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>To investigate the effects of HSYA on FLSs, we exposed FLSs to Interleukin\u20101 beta (IL\u20101\u03b2) and assessed their proliferation via CCK8, scratch, transwell, TUNEL, and flow cytometry assays. Inflammatory cytokine levels were determined by ELISA. The involvement of the MEK\u2010ERK signaling pathway was validated via RT\u2010qPCR and immunofluorescence analyses.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>Treatment with HSYA significantly inhibited FLSs proliferation, while promoting their apoptosis. Moreover, HSYA altered the expression of the inflammatory cytokines IL\u20106, IL\u201010, and TNF\u2010\u03b1 in FLSs. The anti\u2010inflammatory and anti\u2010proliferative effects of HSYA on FLSs were mediated, at least in part, through the inhibition of the ERK signaling pathway.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusion<\/jats:title>\n                    <jats:p>Our findings demonstrate that HSYA induces apoptosis, inhibits proliferation, and suppresses the production of inflammatory cytokines in FLSs via the ERK\/MEK signaling pathway. These findings suggest that HSYA has potential therapeutic value in the treatment of RA and warrants further investigation.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1155\/mi\/7413982","type":"journal-article","created":{"date-parts":[[2026,6,8]],"date-time":"2026-06-08T09:24:37Z","timestamp":1780910677000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":0,"title":["Hydroxysafflor Yellow A Induces Apoptosis and Inhibits Inflammatory Cytokine Expression in Rheumatoid Arthritis Synovial Fibroblasts Through the MEK\u2010ERK Pathway"],"prefix":"10.1155","volume":"2026","author":[{"ORCID":"https:\/\/orcid.org\/0009-0003-0945-7357","authenticated-orcid":false,"given":"Dongwei","family":"Li","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0009-0005-2303-0725","authenticated-orcid":false,"given":"Hongkai","family":"Yang","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0009-0005-0562-9320","authenticated-orcid":false,"given":"Yao","family":"Feng","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0009-0000-8242-3282","authenticated-orcid":false,"given":"Xiaoda","family":"Liu","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0009-0005-0914-7118","authenticated-orcid":false,"given":"Feng","family":"Wang","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0009-0002-1070-7985","authenticated-orcid":false,"given":"Yue","family":"Jiang","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-5311-1324","authenticated-orcid":false,"given":"Suqin","family":"Wu","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-3698-0525","authenticated-orcid":false,"given":"Xifan","family":"Mei","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"311","published-online":{"date-parts":[[2026,6,8]]},"reference":[{"key":"e_1_2_10_1_2","doi-asserted-by":"publisher","DOI":"10.1111\/j.0105-2896.2009.00859.x"},{"key":"e_1_2_10_2_2","doi-asserted-by":"publisher","DOI":"10.1016\/j.intimp.2021.107392"},{"key":"e_1_2_10_3_2","doi-asserted-by":"publisher","DOI":"10.1038\/s41467-023-36468-2"},{"key":"e_1_2_10_4_2","doi-asserted-by":"publisher","DOI":"10.1016\/S0140-6736(17)31472-1"},{"key":"e_1_2_10_5_2","doi-asserted-by":"publisher","DOI":"10.4049\/jimmunol.166.4.2270"},{"key":"e_1_2_10_6_2","doi-asserted-by":"crossref","first-page":"1115","DOI":"10.1002\/1529-0131(200005)43:5<1115::AID-ANR22>3.0.CO;2-A","article-title":"Regulation of Synovial B Cell Survival in Rheumatoid Arthritis by Vascular Cell Adhesion Molecule 1 (CD106) Expressed on Fibroblast-Like Synoviocytes","volume":"43","author":"Reparon-Schuijt C. 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