Effect of selenium yeast combined with vitamin D on thyroid hormone levels and cell apoptosis in Hashimoto′s thyroiditis rat model / 中华内分泌代谢杂志

ABSTRACT

Objective:To explore the effects of selenium yeast combined with vitamin D on thyroid hormone levels and cell apoptosis in Hashimoto′s thyroiditis rat model.Methods:Fifty-five SD rats were divided into control group( n=10) and model group( n=45). Five rats died during the modeling process, and the remaining were divided into model, selenium yeast, vitamin D, and combination therapy groups, with 10 rats in each group. Blood levels of thyroglobulin antibody(TGAb), thyroid peroxidase antibody(TPOAb), thyroid stimulating hormone(TSH), free triiodothyronine(FT 3), free thyroxine(FT 4), tumor necrosis factor α(TNF-α), interleukin(IL)-6, IL-10, IL-17, IL-23, selenium, and vitamin D3 were detected. HE and TUNEL staining were used to observe thyroid tissue morphology and cell apoptosis. Toll-like receptor(TLR)2, TLR4, myeloid differentiation protein 88(MyD88), NF-κB mRNA and protein expressions in thyroid tissue were detected by real-time PCR and Western blotting. Results:Thyroid cells were destroyed and the number of apoptotic cells was increased in model group compared with control group( P<0.05), along with increased levels of TGAb, TPOAb, TSH, TNF-α, IL-6, IL-17, and IL-23 as well as TLR2, TLR4, MyD88, NF-κB mRNA and protein expressions( P<0.05), and decreased FT 3, FT 4, IL-10, selenium, and vitamin D 3 levels( P<0.05). Thyroid cells were relatively normal and the number of apoptotic cells were reduced in the three treatment groups compared with model group( P<0.05), while TGAb, TPOAb, TSH, TNF-α, IL-6, IL-17, IL-23, TLR2, TLR4, MyD88, NF-κB levels were decreased( P<0.05), and FT 3, FT 4, IL-10, selenium, and vitamin D 3 levels were increased( P<0.05), showing the best effect in combination therapy group( P<0.05). Conclusion:Selenium yeast combined with vitamin D attenuates thyroid cell apoptosis, reduces autoimmune damage, and protects thyroid function via inhibiting TLRs/MyD88/NF-κB pathway.