Nurses working with Chinese women should ensure that the information they provide is culturally sensitive, particularly by acknowledging the normative beliefs of this population group.
ObjectiveThis study was aimed to investigate the effects of JiaYanKangTai (JYKT) on regulating interleukin-17 (IL-17) signaling in rats with autoimmune thyroiditis.MethodsLewis rats were administrated with JYKT for eight weeks after a seven-week subcutaneous injection of thyroglobulin with adjuvant and feeding iodine water. Ultrasonography was performed and total volume of thyroid was calculated. The expressions of autoantibodies and hormones were detected. Morphological changes of thyroid were observed. Metabolomics profile and metabolic network analysis were conducted. IL-17 signaling was detected by polymerase chain reaction and immunohistochemistry separately.ResultsJYKT reduced the mean volumes of thyroid, decreased both levels of TPOAb and TGAb, and alleviated lymphocytic infiltration of the thyroid. Metabolic network analysis of metabolomics proved IL-17 signaling pathway as a critical pathway in JYKT administration for autoimmune thyroiditis. JYKT downregulated expressions of IL-17A, TRAF6, p-ERK1/2 and TNF-α.ConclusionJYKT alleviated inflammatory lesions of experimental autoimmune thyroiditis by regulating IL-17 signaling.
Background Autoimmune thyroiditis (AIT) is a common autoimmune disease that causes thyroid dysfunction. Clinical symptoms in Hashimoto thyroiditis patients were improved after oral administration of dioscin. However, the mechanisms involved in the therapeutic effect remain unclear. Methods The protective effects and potential mechanisms of dioscin for autoimmune thyroiditis were explored in a rat model of thyroglobulin-induced autoimmune thyroiditis. Firstly, the rat model of AIT was obtained by subcutaneous injection of thyroglobulin and drinking the sodium iodide solution, followed by gavage administration for 8 weeks. Rats were sacrificed after anaesthesia, serum and thyroid samples were preserved. Serum triiodothyronine (T3), thyroxine (T4), free triiodothyronine (FT3), free thyroxine (FT4), thyrotropin (TSH), thyroglobulin antibody (TgAb), thyroid peroxidase antibody (TPOAb), and thyrotropin receptor antibody (TRAb) expressions were measured by enzyme-linked immunosorbent assay (ELISA). Morphological changes were observed by H&E staining. Next, we used transcriptomics techniques to find the potential therapeutic target of dioscin. Finally, we validated the transcriptomic results by reverse transcription-polymerase chain reaction (RT-PCR) and immunohistochemistry (IHC-P), respectively. Results Animal experiments showed that dioscin regulated T3, T4, FT3, TSH, TgAb, TPOAb, and TRAb and alleviated the pathological process in a dose-dependent manner, with the high-dose group showing optimal efficacy. In the transcriptome, the nuclear factor kappa B (NF-κB) pathway was identified by KEGG enrichment analysis and validated by RT-PCR and IHC-P. The relative expression of NF-κB, mechanistic target of rapamycin (mTOR), and toll-like receptor 4 (TLR4) mRNA and protein were decreased in the dioscin-treated group compared to the AIT model group. Conclusion Our results suggest that dioscin treatment improved thyroid function and downregulated TGAb, TPOAb and TRAb levels in rat models of AIT, which may alleviate the pathological process and suppress the inflammatory response by inhibiting mTOR and TLR4/NF-κB pathways.
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