Abstract
Purpose : To determine the potential influence of diosgenin on proliferation of human thyrocytes and its possible mechanism. Methods : Primary human thyrocytes were cultured and treated with diosgenin at various time intervals. Anti-proliferative activity was determined by MTT assay. Cell proliferation was evaluated by EdU assay while cell cycle was analyzed using fluorescence-activated cell sorting (FACS) method. Protein expression of p21 (CIP1), p27 (KIP1), cyclins, protein kinase B (Akt), phosphatidylinositol 3 kinase (PI3K) and p-Akt was determined by the western blot. Results : Diosgenin inhibited proliferation of primary human thyrocytes and caused G0/G1 arrest in a concentration-dependent manner. It also downregulated cyclin D1 and phosphorylation of PI3K and Akt, but upregulated p21 and p27. Conclusion : Inhibition of proliferation of primary human thyrocytes by diosgenin occurs via downregulation of PI3K/Akt signaling pathway. Therefore, diosgenin can be developed as a potential drug for the treatment of thyroid disease. Keywords : Diosgenin, Proliferation, Primary human thyrocytes, PI3K/Akt signaling pathway
Highlights
Graves’ disease (GD) is a common autoimmune thyroid disease
Diosgenin’s influence on primary human thyrocytes was examined: cell viability was not interrupted significantly when 15 μM of diosgenin was used for 24 h, while 20 μM of diosgenin inhibited cell proliferation (p < 0.001) – a concentration- and time-dependent manner was concluded (Figure 1)
EdU assay was used to examine the influence of diosgenin on cell proliferation
Summary
Graves’ disease (GD) is a common autoimmune thyroid disease. Diffusion of thyroid goiter is a characteristic feature of GD in which cell proliferation is important in the pathogenesis, as the size of thyroid is proportional to the length of time of GD medical treatment [1]. It is important to explore the mechanism for thyroid goiter formation to find effective therapies for GD. Instead of using radioactive iodine and thyroid surgery, antithyroid drugs, including carbimazole, methimazole, and propylthiouracil are the mainstream therapies for uncomplicated GD [2]. There are, drawbacks of these treatments including high recurrence, long treatment course and low remission rate for large goiters. Antithyroid drugs inhibit synthesis of thyroid hormone in large goiter; they
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