Yiqi Jiedu Xiaoying Decoction Improves Experimental Autoimmune Thyroiditis in Rats by Regulating Th17/Treg Cell Balance

Abstract

Background: Experimental autoimmune thyroiditis (EAT) is a widely used animal model to study the pathogenesis and treatment of autoimmune thyroid diseases. Yiqi Jiedu Xiaoying Decoction (YJXD) is a traditional Chinese medicine formula with potential immunomodulatory effects. In this study, we investigated the therapeutic effects of YJXD on EAT in rats and explored its underlying mechanisms. background: The study created a rat model of experimental autoimmune thyroiditis (EAT) to explore the mechanism of Yiqi Jiedu Xiaoying Decoction (YJXD) in the treatment of Hashimoto's thyroiditis (HT). Methods: Female Wistar rats were induced to develop EAT by immunization with thyroglobulin (Tg) and taken sodium iodide water (0.05%) and then treated with YJXD or sodium selenite. HE staining was used to observe the pathological changes of thyroid tissue in EAT rats. Th17 and Treg cell frequencies were analyzed by flow cytometry, and the expression levels of Th17- and Treg-related cytokines and thyroid autoantibody were determined by enzyme-linked immunosorbent assay (ELISA). The expression of Th17- and Treg-related transcriptional factors was detected by real-time polymerase chain reaction (RT-PCR) and Immunohistochemistry (IHC). objective: No Results: Our results demonstrated that treatment with YJXD significantly attenuated the severity of EAT, as evidenced by reduced thyroid gland inflammatory infiltration and decreased serum thyroglobulin autoantibody levels. Importantly, YJXD treatment effectively modulated the Th17/Treg cell balance by suppressing Th17 cell differentiation and promoting Treg cell expansion. Moreover, YJXD was also found to regulate the expression levels of Th17- and Tregrelated cytokines and transcriptional factors, further supporting its immunomodulatory effects in EAT. method: The rat model of EAT was established by subcutaneous injection of porcine thyroglobulin(pTg) combined with high iodine water, and was treated with YJXD and sodium selenite. HE staining was used to observe the pathological changes of thyroid tissue in rats. ELISA were used to detect levels of serum TPOAb, TGAb, interleukin (IL)-17, interleukin (IL)-6, transforming growth factor-β (TGF-β) and interleukin (IL)-10. The percentage of T helper cells 17 (Th17) and regulatory T cells (Treg) of rat spleen mononuclear cells were detected by flow cytometry. The expression of forkhead box P3 (FOXP3), RAR-related orphan receptor gamma T (RORγt) in thyroid tissues of rats were detected by immunohistochemistry. The mRNA expression of Signal Transducer and Activator of Transcription 3 (STAT3), RORγt, FOXP3 and Signal Transducer and Activator of Transcription 5 (STAT5) in spleen was detected by quantitative real-time polymerase chain reaction (qRT-PCR). Conclusion: YJXD exerted therapeutic effects on EAT by regulating the Th17/Treg cell balance, modulating the production of Th17- and Treg-related cytokines and the expression of transcriptional factors. result: In traditional Chinese medicine group, the levels of TPOAb and TGAb decreased and the thyroid inflammation improved. Flow cytometry showed that YJXD increased Treg level, decreased Th17 level and corrected Th17/Treg imbalance in EAT rats. ELISE showed that compared with model group, the expressions of IL-10 and TGF-β in traditional Chinese medicine group increased, while the expressions of IL-17 and IL-6 decreased. IHC showed that the expression of FOXP3 in thyroid tissues of rats increased, while the expression of RORγt decreased. RT-PCR results showed that the mRNA levels of STAT5 and FOXP3 were up-regulated, while the mRNA levels of RORγt and STAT3 were down-regulated. conclusion: YJXD can effectively reduce the level of thyroid antibodies (TPOAb, TGAb), improve thyroid inflammation and regulate Th17/Treg imbalance in EAT rats. The process may be achieved by regulating the level of transcription factors related to Th17 and Treg cells.