Inflammation contributes to osteoarthritis, and cyclin B1 (CCNB1) dysregulation is implicated. Understanding its role and regulation is crucial for developing targeted therapies against this degenerative disease. Mice chondrocytes were acquired from C57BL/6 wild-type mice and treated with interleukin (IL)-1β for inflammation induction, followed by assays for cell viability, apoptosis, inflammatory mediators, cartilage markers, and nuclear factor kappa B (NF-κB) 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-1β-caused decrease in cell viability and increase in apoptosis of chondrocytes. Inflammatory mediators in IL-1β-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-κB inactivation, in chondrocytes administered with IL-1β. Targeting inhibition of CCNB1 reduced the production of inflammation regulators, decreased cartilage degradation, and blocked NF-κB pathway activation. Targeting CCNB1 may serve as a potential therapeutic strategy for osteoarthritis by reducing inflammation, protecting cartilage, and modulating the NF-κB pathway.
Hua et al. (Mon,) studied this question.