{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,28]],"date-time":"2026-10-28T06:45:17Z","timestamp":1793169917642,"version":"4.5.0"},"reference-count":39,"publisher":"Public Library of Science (PLoS)","issue":"4","license":[{"start":{"date-parts":[[2023,4,20]],"date-time":"2023-04-20T00:00:00Z","timestamp":1681948800000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"funder":[{"name":"the Basic Science Research Program through the National Research Foundation of Korea (NRF) funded by the Ministry of Education, Science, and Technology","award":["2018R1A6A1A03025108"],"award-info":[{"award-number":["2018R1A6A1A03025108"]}]},{"name":"the Basic Science Research Program through the National Research Foundation of Korea (NRF) funded by the Ministry of Education, Science, and Technology","award":["2021R1A2C2009782"],"award-info":[{"award-number":["2021R1A2C2009782"]}]},{"name":"Research Fund, 2023 of The Catholic University of Korea"}],"content-domain":{"domain":["www.plosone.org"],"crossmark-restriction":false},"short-container-title":["PLoS ONE"],"abstract":"<jats:p>\n                    Interleukin-1\u03b2 (IL-1\u03b2) is one of the most potent pro-inflammatory cytokines implicated in a wide range of autoinflammatory, autoimmune, infectious, and degenerative diseases. Therefore, many researchers have focused on developing therapeutic molecules that inhibit IL-1\u03b2-IL-1 receptor 1 (IL-1R1) interaction for the treatment of IL-1-related diseases. Among IL-1-related diseases, osteoarthritis (OA), is characterized by progressive cartilage destruction, chondrocyte inflammation, and extracellular matrix (ECM) degradation. Tannic acid (TA) has been proposed to have multiple beneficial effects, including anti-inflammatory, anti-oxidant, and anti-tumor activities. However, it is unclear whether TA plays a role in anti-IL-1\u03b2 activity by blocking IL-1\u03b2-IL-1R1 interaction in OA. In this study, we report the anti-IL-1\u03b2 activity of TA in the progression of OA in both\n                    <jats:italic>in vitro<\/jats:italic>\n                    human OA chondrocytes and\n                    <jats:italic>in vivo<\/jats:italic>\n                    rat OA models. Herein, using-ELISA-based screening, natural compound candidates capable of inhibiting the IL-1\u03b2-IL-1R1 interaction were identified. Among selected candidates, TA showed hindering IL-1\u03b2-IL-1R1 interaction by direct binding to IL-1\u03b2 using surface plasmon resonance (SPR) assay. In addition, TA inhibited IL-1\u03b2 bioactivity in HEK-Blue IL-1-dependent reporter cell line. TA also inhibited IL-1\u03b2-induced expression of inducible nitric oxide synthase (NOS2), cyclooxygenase-2 (COX-2), IL-6, tumor necrosis factor-alpha (TNF-\u03b1), nitric oxide (NO), and prostaglandin E2 (PGE2) in human OA chondrocytes. Moreover, TA downregulated IL-1\u03b2-stimulated matrix metalloproteinase (MMP)3, MMP13, ADAM metallopeptidase with thrombospondin type 1 motif (ADAMTS)4, and ADAMTS5, while upregulating collagen type II (COL2A1) and aggrecan (ACAN). Mechanistically, we confirmed that TA suppressed IL-1\u03b2-induced MAPK and NF-\u03baB activation. The protective effects of TA were also observed in a monosodium iodoacetamide (MIA)-induced rat OA model by reducing pain and cartilage degradation and inhibiting IL-1\u03b2-mediated inflammation. Collectively, our results provide evidence that TA plays a potential role in OA and IL-1\u03b2-related diseases by hindering IL-1\u03b2-IL-1R1 interaction and suppressing IL-1\u03b2 bioactivity.\n                  <\/jats:p>","DOI":"10.1371\/journal.pone.0281834","type":"journal-article","created":{"date-parts":[[2023,4,20]],"date-time":"2023-04-20T14:09:32Z","timestamp":1681999772000},"page":"e0281834","update-policy":"https:\/\/doi.org\/10.1371\/journal.pone.corrections_policy","source":"Crossref","is-referenced-by-count":25,"title":["Tannic acid, an IL-1\u03b2-direct binding compound, ameliorates IL-1\u03b2-induced inflammation and cartilage degradation by hindering IL-1\u03b2-IL-1R1 interaction"],"prefix":"10.1371","volume":"18","author":[{"given":"Hae-Ri","family":"Lee","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Young-Jin","family":"Jeong","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Joong-Woon","family":"Lee","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"JooYeon","family":"Jhun","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Hyun Sik","family":"Na","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Keun-Hyung","family":"Cho","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Seok Jung","family":"Kim","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Mi-La","family":"Cho","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-3295-7205","authenticated-orcid":true,"given":"Tae-Hwe","family":"Heo","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"340","published-online":{"date-parts":[[2023,4,20]]},"reference":[{"issue":"6","key":"pone.0281834.ref001","doi-asserted-by":"crossref","first-page":"1003","DOI":"10.1016\/j.immuni.2013.11.010","article-title":"The interleukin-1 family: back to the future","volume":"39","author":"C Garlanda","year":"2013","journal-title":"Immunity"},{"issue":"2","key":"pone.0281834.ref002","doi-asserted-by":"crossref","first-page":"89","DOI":"10.1038\/nri2691","article-title":"The IL-1 family: regulators of immunity","volume":"10","author":"JE 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