Haobo Li, Shuai Yuan, Zhipeng Yue, Lei Zhang, Shu Chen, Qirong Qian, Qiwei Fu, Yi Chen
{"title":"Suppressive effect of curcumin on apoptosis of articular chondrocytes via regulation on NF-κB pathway and NLRP3 inflammasome.","authors":"Haobo Li, Shuai Yuan, Zhipeng Yue, Lei Zhang, Shu Chen, Qirong Qian, Qiwei Fu, Yi Chen","doi":"10.1007/s10616-024-00695-2","DOIUrl":null,"url":null,"abstract":"<p><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 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.</p>","PeriodicalId":10890,"journal":{"name":"Cytotechnology","volume":"77 2","pages":"52"},"PeriodicalIF":2.0000,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11785841/pdf/","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Cytotechnology","FirstCategoryId":"99","ListUrlMain":"https://doi.org/10.1007/s10616-024-00695-2","RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2025/1/31 0:00:00","PubModel":"Epub","JCR":"Q3","JCRName":"BIOTECHNOLOGY & APPLIED MICROBIOLOGY","Score":null,"Total":0}
引用次数: 0
Abstract
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.
期刊介绍:
The scope of the Journal includes:
1. The derivation, genetic modification and characterization of cell lines, genetic and phenotypic regulation, control of cellular metabolism, cell physiology and biochemistry related to cell function, performance and expression of cell products.
2. Cell culture techniques, substrates, environmental requirements and optimization, cloning, hybridization and molecular biology, including genomic and proteomic tools.
3. Cell culture systems, processes, reactors, scale-up, and industrial production. Descriptions of the design or construction of equipment, media or quality control procedures, that are ancillary to cellular research.
4. The application of animal/human cells in research in the field of stem cell research including maintenance of stemness, differentiation, genetics, and senescence, cancer research, research in immunology, as well as applications in tissue engineering and gene therapy.
5. The use of cell cultures as a substrate for bioassays, biomedical applications and in particular as a replacement for animal models.