摘要
目的:探讨地塞米松对小鼠甲状腺滤泡细胞的增殖及凋亡的影响。方法:取BALB/c小鼠甲状腺组织,以胰酶+Ⅱ胶原酶联合消化组织获得甲状腺滤泡细胞,并以甲状腺球蛋白表达与否判断是否为目的细胞。随后采用不同浓度地塞米松刺激目的细胞,并采用MTT、流式细胞术检测细胞增殖抑制率、凋亡率并对相关凋亡基因表达情况进行分析。结果:胰酶联合Ⅱ型胶原酶处理甲状腺组织可获得稳定传代的甲状腺滤泡上皮细胞,且细胞稳定表达甲状腺球蛋白。同时,不同浓度地塞米松对细胞增殖抑制差异具有统计学意义(F=8.544,P<0.05),且抑制情况与药物作用时间具有交互作用(F=4.532,P<0.05);此外,不同的地塞米松浓度10-6、10-5、10-4mol/L下,细胞凋亡率分别为13.39%±0.79%、17.43%±1.38%、26.42%±1.74%,均与0 mol/L地塞米松细胞凋亡率4.51%±0.06%差异均具有统计学意义(P<0.05,P<0.01),而该差异趋势在凋亡基因表达中仍表现出剂量依赖性。结论:地塞米松可有效抑制小鼠甲状腺滤泡细胞增殖,并通过多种凋亡途径促进细胞凋亡。
Objective： To discuss dexamethasone on proliferation of mouse thyroid follicular cells and apoptosis. Methods：Taken BALB / c mice thyroid tissue to trypsin ＋ Ⅱ collagenase digestion organizations get thyroid follicular cells,and expression of thyroglobulin 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^- 6mol / L,10^- 5mol / L,10^- 4mol / 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.
出处
《中国免疫学杂志》
CAS
CSCD
北大核心
2016年第7期965-969,共5页
Chinese Journal of Immunology
关键词
地塞米松
甲状腺滤泡细胞
增殖
凋亡
Dexamethasone
Thyroid follicular cells
Proliferation
Apoptosis
