<p>Our study probed into how curcumin modulates NF-κB pathway to regulate articular chondrocytes. ATDC5 cells were exposed to varying concentrations of curcumin (0, 10, 20, 50, or 100&#xa0;μM) for 48&#xa0;h, followed by an assessment of curcumin’s cytotoxicity. Cells were also treated with 10&#xa0;ng/ml IL-1β, curcumin, 5&#xa0;μg/L NF-κB inhibitor (PDTC), and 5&#xa0;μM NLRP3 inflammasome inducer (nigericin) for 48&#xa0;h, before cell viability, apoptosis, NF-κB pathway-related proteins, NLRP3 inflammasome-related proteins and inflammatory cytokines were detected. IL-1β treatment notably diminished chondrocyte viability and increased apoptosis, evidenced by elevated level of Bax and cleaved caspase-3, and reduced level of Bcl2, while such expression patterns were reversed by curcumin treatment in a concentration-dependent fashion. Additionally, NF-κB pathway and NLRP3 inflammasome in chondrocytes were activated by IL-1β treatment, but can also be suppressed following curcumin intervention. Furthermore, inhibition of NF-κB pathway curtailed the NLRP3 inflammasome activation and chondrocyte apoptosis, while activation of the NLRP3 inflammasome partially reversed the protective impacts of curcumin against chondrocyte apoptosis. Curcumin inhibits NF-κB pathway, thereby preventing the NLRP3 inflammasome activation and ameliorating IL-1β-induced apoptosis in articular chondrocytes.</p>

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Suppressive effect of curcumin on apoptosis of articular chondrocytes via regulation on NF-κB pathway and NLRP3 inflammasome

  • Haobo Li,
  • Shuai Yuan,
  • Zhipeng Yue,
  • Lei Zhang,
  • Shu Chen,
  • Qirong Qian,
  • Qiwei Fu,
  • Yi Chen

摘要

Our study probed into how curcumin modulates NF-κB pathway to regulate articular chondrocytes. ATDC5 cells were exposed to varying concentrations of curcumin (0, 10, 20, 50, or 100 μM) for 48 h, followed by an assessment of curcumin’s cytotoxicity. Cells were also treated with 10 ng/ml IL-1β, curcumin, 5 μg/L NF-κB inhibitor (PDTC), and 5 μM NLRP3 inflammasome inducer (nigericin) for 48 h, before cell viability, apoptosis, NF-κB pathway-related proteins, NLRP3 inflammasome-related proteins and inflammatory cytokines were detected. IL-1β treatment notably diminished chondrocyte viability and increased apoptosis, evidenced by elevated level of Bax and cleaved caspase-3, and reduced level of Bcl2, while such expression patterns were reversed by curcumin treatment in a concentration-dependent fashion. Additionally, NF-κB pathway and NLRP3 inflammasome in chondrocytes were activated by IL-1β treatment, but can also be suppressed following curcumin intervention. Furthermore, inhibition of NF-κB pathway curtailed the NLRP3 inflammasome activation and chondrocyte apoptosis, while activation of the NLRP3 inflammasome partially reversed the protective impacts of curcumin against chondrocyte apoptosis. Curcumin inhibits NF-κB pathway, thereby preventing the NLRP3 inflammasome activation and ameliorating IL-1β-induced apoptosis in articular chondrocytes.