动物造模 z-bio 2021-09-26 293

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

　　Method: Intervene the inflammation of rat articular chondrocytes with the inflammatory factor TNF-α, add different doses of 1α, 25(OH)2D3, ELISA and Western Blot to normal and inflammatory chondrocytes to detect the supernatant of each cell by the above method Neutralize the changes in the secretion and expression of lubricin in cells, and evaluate the regulatory effect of 1α, 25 (OH) 2D3 on lubricin in rat articular chondrocytes.

　　Result: TNF-α can significantly reduce cell viability, as well as the expression and secretion of rubricin in cells and cell supernatants. 1α, 25 (OH) 2D3 can increase the activity of normal chondrocytes and chondrocytes under inflammatory conditions, but cannot regulate the secretion and expression of erythromycin in the supernatant of normal chondrocytes and cells. For inflamed chondrocytes, 1α, 25 (OH) 2D3 can significantly increase the expression of cell supernatant and intracellular lubricin secretion, and there are specific dose-dependent methods.

　　Conclusion: 1α, 25(OH)2D3 can promote the expression and secretion of lubricin in inflamed cartilage cells, and better protect the cartilage surface.