https://www.selleckchem.com/products/gdc-0068.html
Moreover, miR-222-3p was a target of HOTAIR, and its overexpression and knockdown could suppress and aggravate IL-1β-induced chondrocytes injury. Furthermore, restoring ADAM10, a target gene of miR-222-3p, counteracted the protective role of miR-222-3p upregulation. HOTAIR might contribute to IL-1β-induced chondrocytes death, inflammation, extracellular matrix degradation, and oxidative stress in OA via miR-222-3p/ADAM10 axis. HOTAIR might contribute to IL-1β-induced chondrocytes death, inflammation, extracellular matrix degradation, a
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