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• W3112506543 abstract "Abstract Objective To explore the effect of dexamethasone (Dex) infusion on articular cartilage and the underlying mechanisms in vitro and in vivo . Methods Destabilization of medial meniscus (DMM)-induced OA mouse model was used in this study. The mice with Dex treatment were sacrificed and then the knee joint samples were obtained for pathological analysis. Mouse primary chondrocytes were isolated and cultured in the presence or absence of Dex, which were used for calcification analysis and western blot assay. Results Dex accelerated the loss of articular cartilage matrix in mice, while it aggravated the damage of cartilage in DMM-induced OA model at the late stage. The calcium content in calcified cartilage layer in the joints from Dex treated OA mice was significantly higher than that from control mice. Dex treatment enhanced mineralization of articular cartilage matrix and leaded to massive apoptosis of chondrocytes in OA model. In addition, Dex caused autophagy of chondrocytes in the early stage, which was decreased at the late stage of Dex treatment. Moreover, we found that the effect of Dex on the mineralization of articular cartilage matrix in mice was related to AKT activation. Conclusions Continuous infusion of Dex can enhance the calcification of cartilage via AKT activation and increase chondrocyte apoptosis through inhibiting autophagy, which aggravates the damage of articular cartilage and accelerates the progression of OA in vivo." @default.
• W3112506543 created "2020-12-21" @default.
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• W3112506543 date "2020-09-09" @default.
• W3112506543 modified "2023-09-26" @default.
• W3112506543 title "Continuous infusion of dexamethasone aggravates the damage of cartilage via upregulating p-AKT and impairing articular autophagy in experimental OA model" @default.
• W3112506543 doi "https://doi.org/10.21203/rs.3.rs-71569/v1" @default.
• W3112506543 hasPublicationYear "2020" @default.
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