ArticleMolecular medicine reports2024
Tributyltin chloride induces chondrocyte damage through the activation of NLRP3‑mediated inflammation and pyroptosis.
Article in Molecular medicine reports, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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Who cites it
2 citing papers in PubMed.
- Multimodal modulation of metal-based nanomaterials in osteoarthritis immunotherapy: current landscape and future paradigms.Frontiers in immunology · 2026Review
- The role of GZMA as a target of cysteine and biomarker in Alzheimer's disease, pelvic organ prolapse, and tumor progression.Frontiers in pharmacology · 2024Article
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2 authors.
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Abstract
Tributyltin chloride (TBTC) is known to have effects and mechanisms in various diseases; however, whether TBTC is detrimental to joints and causes osteoarthritis (OA), as well as its underlying mechanism, has not yet been fully elucidated. The present study explored the effects of TBTC on rat chondrocytes, as well as on mouse OA. The toxicity of TBTC toward rat chondrocytes was detected using a lactate dehydrogenase (LDH) leakage assay and cell viability was evaluated using the Cell Counting Kit‑8 assay. The results showed that TBTC decreased the viability of rat chondrocytes and increased the LDH leakage rate in a concentration‑dependent manner. Moreover, compared with in the control group, TBTC increased the expression levels of interleukin (IL)‑1β, IL‑18, matrix metalloproteinase (MMP)‑1, MMP‑13, NLR family pyrin domain containing 3 (NLRP3), caspase‑1, PYD and CARD domain containing, and gasdermin D in chondrocytes. Furthermore, knockdown of NLRP3 reversed the TBTC‑induced increases in LDH leakage and NLRP3 inflammasome‑associated protein levels.
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