Abstract:Thyroid disease is a common endocrine system disease, and its etiology is complex and diverse. At present, research on thyroid diseases is mainly limited to the evaluation of clinical efficacy of drugs with few studies on the pathogenesis of this disease. Therefore, it is important to establish animal models of thyroid diseases for analyzing pathological mechanisms and improving the clinical efficacy of disease treatment. A successful experimental animal model can not only increase disease samples in a short period of time with low cost but also avoid harm to the human body. Furthermore, animal models have the advantage of stability. This review summarizes the method used to establish animal models of thyroid diseases in recent years, such as those for hypothyroidism, hyperthyroidism, hashimoto’s thyroiditis, and thyroid cancer, and analyzes the advantages and disadvantages of various models to provide a theoretical basis for the development of related experiments.

Abstract: Objective To explore the mechanism of miR-214 in immunoregulation of type II alveolar cells infected by Mycobacterium tuberculosis. Methods A549 cells were infected with BCG and H37Rv. qRT-PCR was used to measure the expression levels of miR-214 and FGF9. Western blot was used to measure the expression level of FGF9. SP- A, SP-D, TLR2, TLR4, IL-10, TNF-α, TNF-γ, IL-1β and IL-8 were measure by ELISA. Western blot was used to detect expression of PI3K, AKT and p-AKT. Results Compared with those in cells infected with BCG, expression of miR-214 was increased, and expression of FGF9 was decreased in A549 cells infected with H37Rv. Compared with those in the NC- mimic+oe-NC group, SP-A, SP-D and IL-10 were decreased significantly, TLR2, TLR4, TNF-α, TNF-γ, IL-1β and IL-8 were increased significantly. PI3K and AKT/ p-AKT expression was increased significantly in the miR-214-mimic+oe-NC group, SP-A, SP-D and IL-10 were increased significantly. TLR2, TLR4, TNFα, TNF-γ, IL-1 β and IL-8 were decreased significantly, PI3K and AKT/ p-AKT expression was decreased significantly in the NC mimic+oe-FGF9 group. Compared with those in the NC-mimic+oe-NC group, SP-A, SP-D and IL-10 were increased significantly, TLR2, TLR4, TNF-α, TNF-γ, IL-1 β and IL-8 were decreased significantly. PI3K and AKT/ p-AKT expression was decreased significantly in the miR-214 mimic+oe-FGF9 group. Conclusions miR-214 inhibits FGF9 expression and activates the PI3K/ AKT signaling pathway, which leads to the excessive immune response of type II alveolar cells infected by Mtb and the development of inflammation.