ABSTRACT
<p><b>OBJECTIVE</b>To observe the effect of dexamethasone on the proliferation and apoptosis of embryonic palatal mesenchymal (EPM) cells, and chose a proper concentration of dexamethasone which can effect the ordinary growth of embryonic palatal mesenchymal cells.</p><p><b>METHODS</b>The primary EPM cells were isolated and cultured in vitro, then we did biological assay. EPM cells were treated with different concentration dexamethasone (1 x 10(-9), 1 x 10(-8), 1 x 10(-7) and 1 x 10(-6) mol x L(-1)) respectively. The proliferation of EPM cells was evaluated using MTT method. Apoptosis was examined quantitatively with fluorescein stain.</p><p><b>RESULTS</b>In the condition of blood serum's concentration at 10%, optical density step down following the raise of dexamethasone's concentration. The effect of dexamethasone got to a summit at 3 days. Inhibition rate of dexamethasone at 1 x 10(-6) mol x L(-1) was the highest.</p><p><b>CONCLUSION</b>Dexamethasone at 1 x 10(-6) mol x L(-1) can not only inhibit the growth of the EPM cells, but also will not lead to a large number of cells death. Therefore, this concentration can be used as a reference standard in future research. The most significant drug action time of dexamethason appears at the third day after administration, then the effect became weaken following the drug metabolism.</p>
Subject(s)
Animals , Humans , Mice , Apoptosis , Cell Proliferation , Cells, Cultured , Dexamethasone , In Vitro Techniques , Mesenchymal Stem CellsABSTRACT
<p><b>OBJECTIVE</b>To observe the alteration of fibroblast growth factor 10 (Fgf10) and fibroblast growth factor receptor 2 (Fgfr2b) signal in mouse embryonic palate after dexamethasone and vitamin B12 exposure.</p><p><b>METHODS</b>Dams were divided teratogenetic group, antagomistic group and control group and were respectively injected dexamethasone, dexamethasone and vitamin B12, and normal sodium. Dams were killed and fetus was collected at embryo 12.5 and 13.5 day. The expression of Fgf10 and Fgfr2b and mesenchymal cells proliferation of mouse embryonic by western blotting and BrdU assay were checked.</p><p><b>RESULTS</b>Fgf10 and Fgfr2b expression was down-regulated and mesenchymal cells proliferation was inhibited significantly after dexamethasone exposure. After vitamin B12 treatment, Fgf10 and Fgfr2b expression did not restore, but cells proliferation was recovered.</p><p><b>CONCLUSION</b>Dexamethasone and vitamin B12 affected the expression of Fgf10 and Fgfr2b of mouse embryonic palate and mesenchyme cells proliferation, but the change was disaccord.</p>
Subject(s)
Animals , Mice , Cell Proliferation , Dexamethasone , Fibroblast Growth Factor 10 , Receptor, Fibroblast Growth Factor, Type 2 , Signal Transduction , Vitamin B 12ABSTRACT
Excessive dexamethasone (Dex) administrated into pregnant mice during critical periods of palatal development can produce a high incidence of cleft palate. Its mechanisms remain unknown. Vitamin B12 has been shown to antagonize the teratogenic effects of Dex, which, however, remains controversial. In this study, we investigated the effects of Dex and vitamin B12 on murine embryonic palatal shelf fusion using organ culture of murine embryonic shelves. The explanted palatal shelves on embryonic day 14 (E14) were cultured for 24, 48, 72 or 96 h in different concentrations of Dex and/or vitamin B12. The palatal shelves were examined histologically for the morphological alterations on the medial edge epithelium (MEE) and fusion rates among different groups. It was found that the palatal shelves were not fused at 72 h or less of culture in Dex group, while they were completely fused in the control and vitamin B12-treated groups at 72 and 96 h, respectively. The MEE still existed and proliferated. In Dex+vitamin B12 group the palatal shelves were fused at each time point in a similar rate to controls. These results may suggest that Dex causes teratogenesis of murine embryonic palatal shelves and vitamin B12 prevents the teratogenic effect of Dex on palatogenesis on murine embryos in vitro.