动物造模 z-bio 2022-03-30 501

　　Objective: To investigate the effect of 1α,25(OH)2D3 on the synthesis and secretion of lubricin in chondrocytes at the cellular level.

　　Methods: The inflammatory factor TNF-α was used to intervene inflammation in rat articular chondrocytes, and different doses of 1α, 25(OH)2D3 were added to chondrocytes under normal and inflammatory conditions, respectively. To evaluate the regulation of 1α, 25(OH)2D3 on lubricin in rat articular chondrocytes by neutralizing the changes in the secretion and expression of intracellular lubricin.

　　RESULTS: TNF-α could significantly reduce cell viability, as well as the expression and secretion of lubricin in cells and cell supernatants. 1α,25(OH)2D3 can increase the activity of normal chondrocytes and chondrocytes under inflammation, but cannot regulate the secretion and expression of normal chondrocyte supernatant and intracellular lubricin. For chondrocytes in inflammatory state, 1α, 25(OH) 2D3 can significantly increase the secretion and expression of lubricin in the cell supernatant and in the cell in a dose-dependent manner.

　　Conclusion: 1α,25(OH)2D3 can promote the expression and secretion of chondrocyte lubricin in inflammatory state, so as to better protect the cartilage surface.