Effect of emodin on T cell subsets in NOD mice with NaI‑induced experimental autoimmune thyroiditis.

Chronic lymphocytic thyroiditis (CLT), also known as Hashimoto's thyroiditis, is an autoimmune disease in which the thyroid gland is gradually destroyed. To date, only a limited number of agents can effectively suppress thyroiditis development in CLT patients. The aim of the current study was to investigate the protective effect of emodin on experimental autoimmune thyroiditis (EAT) in mice, which is considered an excellent model for CLT. NaI was used to induce the EAT model in non‑obese diabetic (NOD) mice. An ELISA method was employed to detect the TgAb level (thyroid inflammation) in the serum of the EAT mice. The T cell subsets in peripheral blood and spleen were detected by flow cytometry. The histopathological study revealed that the thyroid inflammatory cell infiltration was significantly reduced by emodin compared with the model group. In addition, ELISA assays indicated that the NaI‑induced serum TgAb upregulation was dramatically revered by emodin. Moreover, the level of serum IFN‑γ and the cell populations of CD3+CD4+IL‑4+, CD3+CD4+ IFN‑γ+, CD3+CD8+IL‑4+, CD3+CD8+ IFN‑γ+ T cells in peripheral blood monocytes and splenic lymphocytes were significantly increased by NaI in the model group compared with in the normal group. Nevertheless, this type of increase was markedly attenuated by emodin. To conclude, the EAT model was successfully established by treating NOD mice with NaI. Emodin indicated an inhibitory effect on the autoimmune response that was significantly different in EAT compared with control mice. Furthermore, the anti‑inflammatory action of emodin on EAT mice may be mediated via the inhibition of the secretion of IFN‑γ and the cell numbers of CD3+CD4+IL‑4+, CD3+CD4+ IFN‑γ+, CD3+CD8+IL‑4+ and CD3+CD8+ IFN‑γ+ T cells in the peripheral blood monocytes and splenic lymphocytes. Therefore, the data may offer valuable insight on the efficacy of treatment of CLT with emodin.