动物造模 z-bio 2022-07-21 272

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

　　Methods: Rat primary chondrocytes were isolated by enzymatic digestion and treated with 10-8, 10-7, 10-6, 10-5 mol/L nicotine for 48 h. The remaining 4 groups were treated with 4 μM MIA for 24 h and given nicotine. MTT method was used to detect chondrocyte viability in each group; Annexin V-FITC/PI flow double staining cytometry was used to detect chondrocyte apoptosis in each group; spectrophotometry was to detect cysteine-containing aspartic acid proteolysis in each group of chondrocytes Enzyme (Caspase 3) activity; Western blot analysis of phosphatidylinositol 3 kinase (PI3K)/protein kinase B (AKT) activation and the expression of downstream target molecules Bax and Bcl-2.

　　Results: 10-7, 10-6 mol/L nicotine significantly promoted rat chondrocyte viability (P < 0.05), 10-5 mol/L nicotine significantly decreased rat chondrocyte viability (P < 0.05), 10-8 mol /L nicotine had no effect on rat chondrocyte viability (P > 0.05). 10-8, 10-7, 10-6 mol/L nicotine can dose-dependently increase MIA-induced rat chondrocyte viability, and inhibit MIA-induced rat chondrocyte apoptosis and Caspase 3 activity (P < 0.05) ;10-7,10-6 mol/L nicotine can increase the expression of PI3K and phosphorylation of AKT, down-regulate the expression of Bax, and up-regulate the expression of Bcl-2 (P < 0.05).

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