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OBJECTIVE: Osteoarthritis (OA) is a common clinical degenerative disease and has a high incidence in the elderly. The purpose of this study was to explore the anti-oxidative stress and anti-aging effects of Peroxiredoxin II (Prx II) on articular chondrocytes, as well as its molecular mechanism. MATERIALS AND METHODS: Articular cartilage tissues and culture human articular chondrocytes were selected. By constructing Prx II overexpressing lentivirus, the effects of Prx II on oxidative stress and cell senescence in chondrocytes were studied. Besides, the p16 overexpression lentivirus was constructed to investigate the effect of Prx II on the p16-CDK4/ 6-pRb-E2F signaling pathway (p16 signaling pathway). RESULTS: Articular cartilage tissues in patients with OA and IL-1β-induced chondrocytes expressed lower Prx II and had higher p16 signaling pathway activity. The overexpression of Prx II significantly increased the expression of SOD1 and SOD2 and decreased the expression of β-gal and P53/P21, indicating that Prx II can reduce the oxidative stress and senescence level of chondrocytes. Moreover, the overexpression of Prx II increased the expression of p16 signaling pathway-related molecules and the activation of the p16 signaling pathway attenuated the anti-oxidative stress and anti-aging effects of Prx II. CONCLUSIONS: Prx II can inhibit the p16 signaling pathway in chondrocytes to reduce the level of aging in chondrocytes, thereby reducing the level of oxidative stress in chondrocytes, and ultimately inhibiting the progression of OA. [ABSTRACT FROM AUTHOR]

OBJECTIVE: To clarify the role of microRNA-183-5p in the malignant progression of osteosarcoma (OS) and the potential mechanism. PATIENTS AND METHODS: Relative level of microRNA-183-5p in 40 paired OS tissues and matched normal tissues was determined by quantitative Real Time-Polymerase Chain Reaction (qRT-PCR). Correlation between microRNA-183-5p level and clinical indexes of OS patients was analyzed. By transfection of microRNA-183-5p mimics in SaOS-2 and MG63 cells, changes in proliferation and migration were evaluated. The potential target of microRNA-183-5p was verified by dual-luciferase reporter gene assay. Finally, the biological function of protein kinase B (AKT) in OS progression mediated by microRNA-183-5p was detected. RESULTS: MicroRNA-183-5p was downregulated in OS tissues compared to controls. Relative to OS patients with high expression of microRNA-183-5p, those with low expression had a higher rate of distant metastasis and lower overall survival. Transfection of microRNA-183-5p mimics attenuated proliferative and migratory abilities of SaOS-2 and MG63 cells. AKT was upregulated in OS and negatively correlated to microRNA-183-5p. Overexpression of AKT could abolish the inhibitory effect of microRNA-183-5p on proliferative and migratory abilities of OS cells. CONCLUSIONS: MicroRNA-183-5p is closely related to distant metastasis and poor prognosis of OS. It suppresses the malignant progression of OS by targeting AKT. [ABSTRACT FROM AUTHOR]