Buzhong Yiqi Decoction alleviates immune injury of autoimmune thyroiditis in NOD.H-2~(h4)mice via c GAS-STING signaling pathway.
10.19540/j.cnki.cjcmm.20241107.703
- Author:
Yi-Ran CHEN
1
;
Lan-Ting WANG
2
;
Qing-Yang LIU
3
;
Zhao-Han ZHAI
2
;
Shou-Xin JU
2
;
Xue-Ying CHEN
3
;
Zi-Yu LIU
4
;
Xiao YANG
4
;
Tian-Shu GAO
3
;
Zhi-Min WANG
5
Author Information
1. College of Acupuncture-Moxibustion and Tuina, Liaoning University of Traditional Chinese Medicine Shenyang 110847, China.
2. the First School of Clinical Medicine, Liaoning University of Traditional Chinese Medicine Shenyang 110847, China.
3. the Affiliated Hospital of Liaoning University of Traditional Chinese Medicine Shenyang 110032, China.
4. the Second Affiliated Hospital of Liaoning University of Traditional Chinese Medicine Shenyang 110034, China.
5. the First School of Clinical Medicine, Liaoning University of Traditional Chinese Medicine Shenyang 110847, China the Affiliated Hospital of Liaoning University of Traditional Chinese Medicine Shenyang 110032, China.
- Publication Type:Journal Article
- Keywords:
Buzhong Yiqi Decoction;
autoimmune thyroiditis;
cyclic guanosine monophosphate-adenosine monophosphate synthase(cGAS)-stimulator of interferon genes(STING) signaling pathway;
immune injury
- MeSH:
Animals;
Drugs, Chinese Herbal/administration & dosage*;
Signal Transduction/drug effects*;
Thyroiditis, Autoimmune/metabolism*;
Mice;
Membrane Proteins/metabolism*;
Mice, Inbred NOD;
Humans;
Female;
Nucleotidyltransferases/metabolism*;
Male;
Disease Models, Animal
- From:
China Journal of Chinese Materia Medica
2025;50(7):1872-1880
- CountryChina
- Language:Chinese
-
Abstract:
This study aims to explore the effects of Buzhong Yiqi Decoction(BYD) on the cyclic guanosine monophosphate-adenosine monophosphate synthase(cGAS)-stimulator of interferon genes(STING) signaling pathway in the mouse model of autoimmune thyroiditis(AIT) and the mechanism of BYD in alleviating the immune injury. Forty-eight NOD.H-2~(h4) mice were assigned into normal, model, low-, medium-, and high-dose BYD, and selenium yeast tablets groups(n=8). Mice of 8 weeks old were treated with 0.05% sodium iodide solution for 8 weeks for the modeling of AIT and then administrated with corresponding drugs by gavage for 8 weeks before sampling. High performance liquid chromatography was employed to measure the astragaloside Ⅳ content in BYD. Hematoxylin-eosin staining was employed to observe the pathological changes in the mouse thyroid tissue. Enzyme-linked immunosorbent assay was employed to measure the serum levels of thyroid peroxidase antibody(TPO-Ab), thyroglobulin antibody(TgAb), and interferon-γ(IFN-γ). Flow cytometry was employed to detect the distribution of T cell subsets in the spleen. The immunohistochemical method was used to detect the expression of cGAS, STING, TANK-binding kinase 1(TBK1), and interferon regulatory factor 3(IRF3). Real-time PCR and Western blot were employed to determine the mRNA and protein levels, respectively, of markers related to the cGAS-STING signaling pathway in the thyroid tissue. The results showed that the content of astragaloside Ⅳ in BYD was(7.06±0.08) mg·mL~(-1). Compared with the normal group, the model group showed disrupted structures of thyroid follicular epithelial cells, massive infiltration of lymphocytes, and elevated levels of TgAb and TPO-Ab. Compared with the model group, the four treatment groups showed intact epithelial cells, reduced lymphocyte infiltration, and lowered levels of TgAb and TPO-Ab. Compared with the normal group, the model group showed increases in the proportions of Th1 and Th17 cells, a decrease in the proportion of Th2 cells, and an increase in the IFN-γ level. Compared with the model group, the four treatment groups presented decreased proportions of Th1 and Th17 cells and lowered levels of IFN-γ, and the medium-dose BYD group showed an increase in the proportion of Th2 cells. Compared with the normal group, the modeling up-regulated the mRNA levels of cGAS, STING, TBK1, and IRF3 and the protein levels of cGAS, p-STING, p-TBK1, and p-IRF3. Compared with the model group, the four treatment groups showed reduced levels of cGAS, STING, TBK1, and IRF3-positive products, down-regulated mRNA levels of cGAS, STING, and TBK1, and down-regulated protein levels of cGAS and p-STING. The high-dose BYD group showed down-regulations in the mRNA level of IRF3 and the protein levels of p-TBK1 and p-IRF3. The above results indicate that BYD can repair the imbalance of T cell subsets, alleviate immune injury, and reduce thyroid lymphocyte infiltration in AIT mice by inhibiting the cGAS-STING signaling pathway.
