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Arch Pharm Res ; 34(6): 997-1005, 2011 Jun.
Article in English | MEDLINE | ID: mdl-21725821

ABSTRACT

Others and our previous studies showed that the increase of IGF-1 was involved in the formation of goiter. Our aim here was to evaluate the possible effects of diosgenin on cell proliferation induced by IGF-1 in primary human thyroid cells. The cells were treated with or without different concentrations of diosgenin in the present or absent of IGF-1 for 24, 48 and 72 h, respectively. Cell viability was determined by MTT, and cell proliferation was tested by EdU assay, and cell cycle analysis was performed by FACS. In addition, Cyclin D1 and B1 protein expression was tested by Western Blotting, respectively. We found that IGF-1 promoted cell cycle progression to S phase and increased the primary human thyroid cells proliferation. Diosgenin decreased the protein expression of cyclin D1 and resulted in cell G(0)/G(1) arrest. Importantly, when the human thyrocytes were exposed to diosgenin in the present of IGF-1, the IGF-1 inducing proliferation was significantly decreased and the proportion of the cells in G(0)/G(1) phase was increased, while that of S phase was decreased. This study shows that diosgenin inhibited cell proliferation, caused G(0)/G(1) arrest, and could inhibit cell proliferation induced by IGF-1 in primary human thyroid cells.


Subject(s)
Cell Proliferation/drug effects , Diosgenin/pharmacology , Insulin-Like Growth Factor I/pharmacology , Thyroid Gland/drug effects , Blotting, Western , Cell Cycle/drug effects , Cell Survival/drug effects , Cells, Cultured , Cyclin B1/genetics , Cyclin D1/genetics , Diosgenin/administration & dosage , Dose-Response Relationship, Drug , G1 Phase/drug effects , Gene Expression Regulation/drug effects , Humans , Resting Phase, Cell Cycle/drug effects , Thyroid Gland/cytology , Time Factors
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