【Animal modeling】-1,25(OH)2 D3 protects thyroid function in rats with experimental autoimmune thyroiditis by inhibiting TLR2/NF-κB signaling pathway

  Objective To study the protective mechanism of 1,25(OH)2D3 on experimental autoimmune thyroiditis rats based on TLR2/NF-κB signaling pathway.

  Methods Rats were randomly divided into control group, model group, selenium yeast tablet control group and 1,25(OH)2D3 low, medium and high dose groups. Except for the control group, the other rats were given subcutaneous injection of thyroglobulin (PTg) to establish the autoimmune thyroiditis rat model, and the 1,25(OH)2D3 low, medium and high dose groups were given intraperitoneal injection of 0.5, 1 0, 1.5 μg/kg 1,25(OH)2D3 injection, the control group and model group were injected with the same amount of distilled water, and the selenium yeast tablet control group was injected with the same amount of selenium yeast suspension (once a day) for 4 consecutive weeks . The changes of thyroid tissue in rats were observed, and the contents of thyroid function factors, serum inflammatory factors, thyroid autoantibodies, and the levels and gene expressions of TLR2/NF-κB signaling pathway-related proteins were detected.

  Results Compared with the rats in the model group, the levels of serum free triiodothyronine (FT3), free thyroxine (FT4), thyroid stimulating hormone (TSH), thyroglobulin antibody, and thyroglobulin antibody in the 1,25(OH)2D3 groups were (TGAb), Thyroid Peroxidase Antibody (TPOAb), Interleukin-6 (IL-6), Interleukin-12 (IL-12), Tumor Necrosis Factor-α (TNF-α) and Thyroid TLR2 , MyD88, TRAF-6 and NF-κB mRNA and protein expressions were decreased to varying degrees, while interleukin-10 (IL-10) increased to varying degrees, and the difference between the high-dose 1,25 ( OH) 2D3 group and the model group was statistically significant academic significance (P < 0.05).

  Conclusion 1,25(OH)2D3 can improve the thyroid function of rats with autoimmune thyroiditis to a certain extent, and can increase the level of autoimmune antibodies. The mechanism may be related to the inhibition of TLR2/NF-κB by 1,25(OH)2D3. Signal pathway activity, thereby regulating the release of inflammatory factors such as IL-6, IL-10, IL-12 and TNF-α.