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Tannic acid, an IL-1[beta]-direct binding compound, ameliorates IL-1[beta]-induced inflammation and cartilage degradation by hindering IL-1[beta]-IL-1R1 interaction

PloS one, 2023-04, Vol.18 (4), p.e0281834 [Peer Reviewed Journal]

COPYRIGHT 2023 Public Library of Science ;ISSN: 1932-6203 ;EISSN: 1932-6203 ;DOI: 10.1371/journal.pone.0281834

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  • Title:
    Tannic acid, an IL-1[beta]-direct binding compound, ameliorates IL-1[beta]-induced inflammation and cartilage degradation by hindering IL-1[beta]-IL-1R1 interaction
  • Author: Lee, Hae-Ri ; Jeong, Young-Jin ; Lee, Joong-Woon ; Jhun, JooYeon ; Na, Hyun Sik ; Cho, Keun-Hyung ; Kim, Seok Jung ; Cho, Mi-La ; Heo, Tae-Hwe
  • Subjects: Health aspects ; Interleukin-1 ; Tannins
  • Is Part Of: PloS one, 2023-04, Vol.18 (4), p.e0281834
  • Description: Interleukin-1[beta] (IL-1[beta]) 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[beta]-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[beta] activity by blocking IL-1[beta]-IL-1R1 interaction in OA. In this study, we report the anti-IL-1[beta] activity of TA in the progression of OA in both in vitro human OA chondrocytes and in vivo rat OA models. Herein, using-ELISA-based screening, natural compound candidates capable of inhibiting the IL-1[beta]-IL-1R1 interaction were identified. Among selected candidates, TA showed hindering IL-1[beta]-IL-1R1 interaction by direct binding to IL-1[beta] using surface plasmon resonance (SPR) assay. In addition, TA inhibited IL-1[beta] bioactivity in HEK-Blue IL-1-dependent reporter cell line. TA also inhibited IL-1[beta]-induced expression of inducible nitric oxide synthase (NOS2), cyclooxygenase-2 (COX-2), IL-6, tumor necrosis factor-alpha (TNF-[alpha]), nitric oxide (NO), and prostaglandin E2 (PGE2) in human OA chondrocytes. Moreover, TA downregulated IL-1[beta]-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[beta]-induced MAPK and NF-[kappa]B 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[beta]-mediated inflammation. Collectively, our results provide evidence that TA plays a potential role in OA and IL-1[beta]-related diseases by hindering IL-1[beta]-IL-1R1 interaction and suppressing IL-1[beta] bioactivity.
  • Publisher: Public Library of Science
  • Language: English
  • Identifier: ISSN: 1932-6203
    EISSN: 1932-6203
    DOI: 10.1371/journal.pone.0281834
  • Source: Public Library of Science (PLoS) Journals Open Access
    GFMER Free Medical Journals
    PubMed Central
    ProQuest Central
    DOAJ Directory of Open Access Journals
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