Background Osteoarthritis (OA) is one kind of degenerative joint disease that happens in articular cartilage and other joint tissues. Long non-coding RNAs (lncRNAs) have been reported to serve as pivotal regulators in many diseases, including OA. However, the role and relevant regulatory mechanisms of CASC19 in OA remain unknown. Methods The expression levels of CASC19, miR-152-3p, and DDX6 were identified by reverse-transcription polymerase chain reaction (RT-qPCR). Cell viability and apoptosis were determined by Cell Counting Kit-8 (CCK-8) and flow cytometry assays, respectively. The relationship between miR-152-3p and CASC19 or DDX6 was predicted by bioinformatics tools and verified by the dual-luciferase reporter assay. Results CASC19 was verified to exhibit higher expression in OA tissues and cells. Moreover, inhibition of CASC19 weakened proinflammatory cytokine (IL-6, IL-8, and TNF-α) production and cell apoptosis but facilitated cell viability. Experiments of the ceRNA mechanism elucidated that miR-152-3p was a sponge for CASC19, and miR-152-3p targeted DDX6, suggesting that CASC19 sponged miR-152-3p to release DDX6. Finally, results from rescue assays proved that the impacts of CASC19 silencing on chondrocytes apoptosis and proinflammatory cytokine production could be reversed by DDX6 overexpression. Conclusions It was concluded that lncRNA CASC19 accelerated chondrocytes apoptosis and proinflammatory cytokine production to exacerbate osteoarthritis development through regulating the miR-152-3p/DDX6 axis. These findings may offer an effective biological target for OA treatment.

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Mixed ligand of H2ip and L assembled with Zn(NO3)2 ·6H2O under solvothermal conditions provided a novel Zn(II) compound formulated as [Zn(ip)(L)] (1, H2ip = isophthalic acid, L is 4-[4-(1H-imidazol-1-yl)phenyl]-2, 6-bis(pyridin-4-yl)pyridine). This compound’s emission performances in solid state were also explored at RT. In the biological section, the as-created complex’s application values against tendon bone healing were discussed, and the mechanism was researched simultaneously. First, activation of the Wnt signaling pathway in bone tissue was examined by real-time reverse transcription-polymerase chain reaction. Second, quantitative computed tomography was performed to measure the bone density of the animal after compound treatment.