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Catalpol protects mouse ATDC5 chondrocytes against interleukin-1β-induced catabolism

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dc.contributor.authorCai, Chengkui
dc.contributor.authorSun, Pengcheng
dc.contributor.authorChen, Zhihui
dc.contributor.authorSun, Chao
dc.contributor.authorTian, Liying
dc.date.accessioned2024-02-07T09:28:15Z
dc.date.available2024-02-07T09:28:15Z
dc.date.issued2024
dc.description.abstractCatalpol is a natural product with promising anti-inflammatory effects, however, its effects on chondrocytes and osteoarthritis (OA) have not been well investigated. OA is a painful and debilitating joint disease that affects people worldwide. Traditional Chinese Medicine has been sought to treat OA, including the Rehmannia extract, Catalpol. Here, we examined the effects of Catalpol, a plant derivative used in traditional Chinese medicine, on ATDC5 chondrocytes originating from mouse teratocarcinoma cells stimulated with interleukin-1β (IL-1β) to mimic the OA cellular environment. Catalpol significantly reduced matrix metalloproteinase-1, -3, -13 (MMP-1, -3, -13), a disintegrin and metalloproteinase with thrombospondin motifs -4, -5 (ADAMTS-4, -5) against IL-1β, demonstrating a likely anti-cartilage degradation activity. We also found that Catalpol exerted a significant antioxidative stress effect by downregulating the production of inducible nitric oxide synthase (iNOS), nitric oxide (NO), reactive oxygen species (ROS), and malondialdehyde (MDA). Catalpol treatment significantly reduced the levels of several key inflammatory factors, including Prostaglandin E2 (PGE2), cyclooxygenase-2 (COX-2), interleukin-8 (IL8), and monocyte chemoattractant protein-1 (MCP-1). We further demonstrate that the effects of Catalpol were mediated by the nuclear factor -κB (NF-κB) pathway via downregulation of the phosphorylation of inhibitor of nuclear factor κB-α (IκBα). This was confirmed by measuring p38 and p65 protein levels as well as the luciferase activity of NF-κB. Altogether, we demonstrate the potential of Catalpol as a novel treatment agent against cartilage matrix degradation, oxidative stress, and inflammation in OA.es
dc.formatapplication/pdfes
dc.format.extent12es
dc.identifier.citationHistology and Histopathology Vol. 39, nº3 (2024)
dc.identifier.doihttps://doi.org/10.14670/HH-18-575
dc.identifier.issn0213-3911
dc.identifier.issn1699-5848
dc.identifier.urihttp://hdl.handle.net/10201/138861
dc.languageenges
dc.publisherUniversidad de Murcia, Departamento de Biologia Celular e Histiologiaes
dc.relationSin financiación externa a la Universidades
dc.rightsinfo:eu-repo/semantics/openAccesses
dc.rightsAttribution-NonCommercial-NoDerivatives 4.0 Internacional*
dc.rights.urihttp://creativecommons.org/licenses/by-nc-nd/4.0/*
dc.subjectCatalpoles
dc.subjectOsteoarthritises
dc.subjectMatrix metalloproteinaseses
dc.subjectADAMTSes
dc.subjectNF-κBes
dc.subject.otherCDU::6 - Ciencias aplicadas::61 - Medicina::616 - Patología. Medicina clínica. Oncologíaes
dc.titleCatalpol protects mouse ATDC5 chondrocytes against interleukin-1β-induced catabolismes
dc.typeinfo:eu-repo/semantics/articlees
dspace.entity.typePublicationes
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Histology and histopathology Vol.39, nº3 (2024)