摘要
目的探讨在桥本甲状腺炎(HT)中白细胞介素-1β(IL-1β)诱导甲状腺细胞凋亡及其可能的作用机制。方法①不同浓度、不同时间IL-1β刺激大鼠甲状腺细胞系(FRTL-5细胞),采用实时荧光定量PCR方法检测FRTL-5细胞自杀因子(Fas)mRNA的表达。②设立对照组、IL-1β组、IL-1β+caspase-8抑制剂(Z-IETD-FMK)组,采用流式细胞术检测各组的甲状腺细胞凋亡率。结果①定量PCR结果显示IL-1β与FRTL-5细胞Fas mRNA表达水平存在剂量-时间依赖关系,差异有统计学意义(P<0.05);②流式细胞术结果显示,与对照组比较,IL-1β作用后,甲状腺细胞的凋亡率增加(P<0.05);联合加入Z-IETD-FMK后,可抑制IL-1β诱导甲状腺细胞凋亡率的增加(P<0.05)。结论IL-1β可能通过Fas和caspase-8途径导致甲状腺细胞的凋亡。
Objective To investigate the interleukin-1β(IL-1β)induced apoptosis of thyroid cells in Hashimoto thyroiditis(HT)and its potential mechanism.Methods①Factor associated suicide(Fas)mRNA expression in FRTL-5 cells were detected by real-time PCR under different concentration and reacting time of IL-1β.②The con-trol group,IL-1βgroup,IL-1β+caspase8 inhibitor(Z-IETD-FMK)group were set up,and the apoptosis rate of each group was analysed by flow cytometry.Results①The result of real-time PCR showed that there was a dose-time dependent relationship between IL-1βand Fas mRNA expression levels of FRTL-5 cells(P<0.05);②Flow cytometry results showed that compared with the control group,the apoptosis rate of thyroid cells increased after IL-1βinduction(P<0.05)and the increase of IL-1β-induced thyroid cell apoptosis was inhibited after combined with Z-IETD-FMK(P<0.05).Conclusion IL-1βmay induce apoptosis of thyroid cells through Fas and caspase 8 pathways.
作者
李阿楠
张晓序
任翠平
沈际佳
左春林
Li Anan;Zhang Xiaoxu;Ren Cuiping(Dept of Endocrinology,The First Affiliated Hospital of Anhui Medical University,Hefei 230022;Dept of Microbiology and Parasitology,School of Basic Medical Sciences,Anhui Medical University,Hefei 230032)
出处
《安徽医科大学学报》
CAS
北大核心
2020年第9期1385-1388,共4页
Acta Universitatis Medicinalis Anhui
基金
国家自然科学基金(编号:81270864)。