Dexamethasone thyroid follicular cell proliferation and apoptosis in mice and its mechanisms / 中国免疫学杂志

ABSTRACT

Objective:To discuss dexamethasone on proliferation of mouse thyroid follicular cells and apoptosis. Methods:Taken BALB/c mice thyroid tissue to trypsin+Ⅱcollagenase digestion organizations get thyroid follicular cells,and expression of thyro-globulin determined whether or not the target cell. Then different concentrations of dexamethasone to stimulate target cells,and the use of MTT,flow cytometry cell proliferation rate,apoptosis rate and the apoptosis-related gene expression analysis. Results: Trypsin joint type Ⅱ collagenase treatment of thyroid tissue to obtain a stable passage of thyroid follicular epithelial cells,and cells stably expressing thyroglobulin. At the same time, different concentrations of dexamethasone on cell proliferation difference was statistically significant (F=8. 544, P<0. 05 ), and the suppression of drug action have interaction ( F = 4. 532, P<0. 05 );in addition, differently dexamethasone concentration 10-6 mol/L, 10-5 mol/L, 10-4 mol/L, the apoptosis rates were 13. 39% ± 0. 79%, 17. 43% ± 1. 38%, 26. 42%±1. 74%,both with 0 mol/L to plug betamethasone 4. 51%± 0. 06% apoptosis rate differences were statistically significant (P<0. 05,P<0. 01),while the difference in the expression of apoptotic genes trend still showed a dose-dependent manner. Conclusion:Dexamethasone can effectively inhibit thyroid follicular cell proliferation and induce apoptosis through a variety of apoptotic pathways.