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Mice chondrocytes were acquired from C57BL\/6 wild-type mice and treated with interleukin (IL)-1\u03b2 for inflammation induction, followed by assays for cell viability, apoptosis, inflammatory mediators, cartilage markers, and nuclear factor kappa B (NF-\u03baB) pathway. CCNB1 was knocked down or upregulated in chondrocytes, respectively. The modified Hulth method was used to establish osteoarthritis model. The knee joint was visualized using micro-computed tomography, and histopathologic evaluation was carried out by immunohistochemistry staining, Safranin O\/fast green, and hematoxylin and eosin staining for cartilage degradation markers. CCNB1 knockdown inhibited IL-1\u03b2-caused decrease in cell viability and increase in apoptosis of chondrocytes. Inflammatory mediators in IL-1\u03b2-treated chondrocytes were decreased after CCNB1 knockdown. CCNB1 knockdown reduced the expression of MMP-13 and ADAMTS-5, while elevated collagen II and aggrecan accumulation, alongside with NF-\u03baB inactivation, in chondrocytes administered with IL-1\u03b2. Targeting inhibition of CCNB1 reduced the production of inflammation regulators, decreased cartilage degradation, and blocked NF-\u03baB pathway activation. Targeting CCNB1 may serve as a potential therapeutic strategy for osteoarthritis by reducing inflammation, protecting cartilage, and modulating the NF-\u03baB pathway.<\/jats:p>","DOI":"10.1369\/00221554251410643","type":"journal-article","created":{"date-parts":[[2026,2,24]],"date-time":"2026-02-24T06:59:25Z","timestamp":1771916365000},"page":"235-248","update-policy":"https:\/\/doi.org\/10.1177\/sage-journals-update-policy","source":"Crossref","is-referenced-by-count":2,"title":["Targeting CCNB1 Repressed Cartilage Degradation Induced by Inflammation Through NF-\u03baB Pathway in Osteoarthritis"],"prefix":"10.1369","volume":"74","author":[{"given":"Hua","family":"Li","sequence":"first","affiliation":[{"name":"School of Basic Medical Sciences, North China University of Science and Technology, Tangshan, China"},{"name":"Hebei Key Laboratory for Chronic Diseases, Tangshan, China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yuxue","family":"Qiao","sequence":"additional","affiliation":[{"name":"School of Basic Medical Sciences, North China University of Science and Technology, Tangshan, China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0009-0009-1493-190X","authenticated-orcid":false,"given":"Mengshuang","family":"Ding","sequence":"additional","affiliation":[{"name":"School of Basic Medical Sciences, North China University of Science and Technology, Tangshan, China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0009-0004-2494-525X","authenticated-orcid":false,"given":"Yirong","family":"Liu","sequence":"additional","affiliation":[{"name":"School of Basic Medical Sciences, North China University of Science and Technology, Tangshan, China"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"179","published-online":{"date-parts":[[2026,2,23]]},"reference":[{"issue":"9","key":"e_1_3_2_2_2","article-title":"The global burden of osteoarthritis: past and future perspectives","volume":"5","author":"Wong AY","year":"2023","unstructured":"Wong AY, Samartzis D, Maher C. 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