PI3K/AKT/mTOR signaling pathway participates in thyroid autoimmune injury of EAT mice by regulating Th17 cells differentiation
10.12007/j.issn.0258-4646.2024.11.003
- VernacularTitle:PI3K/AKT/mTOR信号通路通过调控Th17细胞分化参与EAT小鼠甲状腺自身免疫损伤
- Author:
Chengyan HE
1
;
Yiwen LI
;
Ling GAN
;
Jue WANG
;
Haibo XUE
Author Information
1. 滨州医学院附属医院内分泌科,山东滨州 256603
- Keywords:
PI3K/AKT/mTOR;
Th17 cell;
autoimmune thyroiditis
- From:
Journal of China Medical University
2024;53(11):972-978
- CountryChina
- Language:Chinese
-
Abstract:
Objective To explore the role and mechanism of phosphatidylinositol 3-kinase/protein kinase B/mechanistic target of rapamycin kinase(PI3K/AKT/mTOR)signaling in autoimmune thyroiditis(AIT).Methods 24 female C57BL/6 mice were randomly divided into four groups:a normal control(NC)group,an experimental autoimmune thyroiditis(EAT)group,and two groups treated with LY294002(25 mg/kg or 50 mg/kg LY294002).The degree of thyroiditis was observed by hematoxylin and eosin staining.The percentage of Th 17 cells in the spleen mononuclear cells(SMCs)was determined by flow cytometry.Enzyme-linked immunosorbent assay was used to measure the concentrations of thyroglobulin antibody(TgAb)and interleukin-17A(IL-17A)in the serum.Western blotting was conducted to detect the protein levels of IL-17A,p-AKT(Thr308),p-AKT(Ser473),p-mTOR(Ser2448),S6K1,and S6K2 in the different groups.Results Compared with the NC group,the infiltration of Th17 cells and the expressions ofIL-17A,p-AKT(Ser473),p-AKT(Thr308),p-mTOR(Ser2448),S6K1,and S6K2 rose remarkably in EAT mice.After the PI3K pathway was blocked,the degree of thyroiditis was significantly alleviated,followed by the proportion of Th17 cells,and the expression of IL-17A and PI3K pathway-related molecules decreased in a dose-dependent manner.Conclusion PI3K/AKT/mTOR signaling pathway participates in thyroid autoimmune jnjury of EAT mice by regulating Th17 cells differentiation.
