Vitamin B12 Counteracts Dexamethasone-Induced Proliferation and Apoptosis During Key Periods of Palatogenesis in Mice
Vitamin B12 Counteracts Dexamethasone-Induced Proliferation and Apoptosis During Key Periods of Palatogenesis in Mice
复制标题
维生素 B12 对抗地塞米松诱导的小鼠腭发育关键时期的增殖和凋亡
DOI：
10.1097/sap.0b013e3181b4bc8d
复制
发表时间：
2010-04-01
影响因子：
1.5
通讯作者：
Shi, Bing
中科院分区：
文献类型：
--
作者：
He, Wei;Meng, Tian;Shi, Bing
B族维生素挽救糖皮质激素诱导的腭裂在啮齿动物，然而，这种效果的机制仍然在很大程度上未知。本研究的目的是评估地塞米松和维生素B-12对腭裂发生过程中细胞增殖和凋亡的影响。在我们的研究中，当受试者在胚胎第13.5天（E13.5）给予地塞米松时，小鼠胚胎腭中的间充质细胞增殖减少。然而，与对照组相比，在E 14.0和E 14.5时地塞米松暴露后间充质细胞增殖增加。维生素B-12处理后，间充质细胞的增殖恢复。对照组和维生素B-12处理组在双侧腭突粘连形成中膜上皮缝前未见细胞凋亡。而地塞米松处理后，在腭接触前，在中缘上皮下检测到凋亡细胞。结果表明，维生素B-12恢复了增殖，地塞米松通过延迟细胞周期和凋亡降低了增殖。本研究提示，在胚胎腭裂发生过程中，维生素B-12可用于预防或减轻地塞米松诱导的腭裂。
B vitamins rescue cleft palate induced by glucocorticoids in rodents; however, the mechanism of this effect remains largely unknown. The objective of our study was to assess the effect of dexamethasone and Vitamin B-12 on cell proliferation and apoptosis during palatogenesis. In our study, mesenchymal cell proliferation in mouse embryonic palates decreased when the subjects were administered dexamethasone at embryo day 13.5 (E 13.5). However, mesenchymal cell proliferation was increased after dexamethasone exposure at E 14.0 and E 14.5 in comparison with the control group. After Vitamin B-12 treatment, proliferation of mesenchymal cells was restored. No apoptosis was detected until bilaterial palatal shelves adhered and formed a medial epithelium seam in the control group and Vitamin B-12-treated group. However, the apoptotic cells were detected under the medial edge epithelium before the palate contacted after dexamethasone treatment. The results suggested that Vitamin B-12 restored proliferation, which had been reduced by dexamethasone via a delayed cellular cycle and apoptosis. This study implies that Vitamin B-12 may be used to prevent or alleviate cleft palate induced by dexamethasone during embryonic palatogenesis.