动物实验,尼古丁,骨关节炎 z-bo 2020-08-24 602

　　Objective: To investigate the inhibitory effect of nicotine on the apoptosis of osteoarthritis chondrocytes induced by sodium iodoacetate (MIA).

　　Methods: The rat primary chondrocytes were isolated by enzyme digestion, and the cells were treated with 10-8, 10-7, 10-6, 10-5 mol/L nicotine for 48 hours, and then removed from the normal group. The remaining 4 groups were treated with 4μMMIA Treated for 24 hours and treated with nicotine. MTT method detects the viability of each group of chondrocytes, Annexin V-FITC/PI flow cytometry detects the apoptosis of each group of chondrocytes, and spectroscopic method detects the cysteine aspartate-containing proteolytic enzyme in each group of chondrocytes Photometric (Caspase3) activity; Western blot analysis of phosphatidylinositol 3-kinase (PI3K)/protein kinase B (AKT) activation and downstream target molecules Bax and Bcl-2 expression.

　　Results: 10-7, 10-6 mol/L nicotine can significantly improve the viability of rat chondrocytes (P0.05). 10-8,10-7,10-6mol/L nicotine dose-dependently increased MIA-induced rat chondrocyte viability and inhibited MIA-induced rat chondrocyte apoptosis and Caspase3 activity (P\u003c0.05); 10 -7,10-6 mol/L nicotine can increase PI3K expression and AKT phosphorylation, down-regulate and promote Bax expression, and up-regulate Bcl-2 expression.

　　Conclusion: A certain dose of nicotine can significantly inhibit the apoptosis of rat chondrocytes induced by MIA, which may be related to the PI3K/AKT signaling pathway.