ArticleCytotechnology2025
The mechanism of curcumin protecting against IL-1β-induced oxidative stress and inflammation in chondrocytes via the Bmp2/Smad5/Runx2 pathway.
Article in Cytotechnology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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1 citing paper in PubMed.
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8 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
A core role of chondrocyte survival/death has been suggested in the pathogenesis of osteoarthritis. We explored the underlying molecular mechanism of curcumin protecting against interleukin-1β (IL-1β)-induced chondrocyte injury via the bone morphogenetic protein 2 (Bmp2)/small mothers against decapentaplegic homolog 5 (Smad5)/runt-related transcription factor 2 (Runx2) pathway. Chondrocytes ATDC5 in vitro inflammatory model was established by IL-1β induction, and treated with curcumin, or Smad5 small interfering RNA. Levels of extracellular matrix (ECM) type II collagen (Col-II) and aggrecan, reactive oxygen species (ROS), superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px), and cyclooxygenase-2 (COX-2), tumor necrosis factor-α (TNF-α) and IL-6 were determined by immunocytochemistry, kits and ELISA. Apoptosis and necrosis were assessed by Annexin V/PI and TUNEL. Matrix metalloproteinase 13 (MMP13), A disintegrin and metalloproteinase with thrombospondin 5 (ADAMTS5), Bmp2/Smad5/Runx2 expression and Smad5 phosphorylation levels were determined by qPCR and western blot. IL-1β-treated ATDC5 cells showed decreased Col-II, aggrecan in ECM and SOD and GSH-Px levels, as well as increased apoptosis and levels of MMP13, ADAMTS5, Bmp2, Runx2, ROS, COX-2, TNF-α and IL-6 and Smad5 phosphorylation (all
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