MYOINOSITOL AND PROSTAGLANDINS REVERSE THE GLUCOSE INHIBITION OF NEURAL-TUBE FUSION IN CULTURED MOUSE EMBRYOS
MYOINOSITOL AND PROSTAGLANDINS REVERSE THE GLUCOSE INHIBITION OF NEURAL-TUBE FUSION IN CULTURED MOUSE EMBRYOS
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DOI：
10.1007/bf00400202
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发表时间：
1990-10-01
期刊：
影响因子：
8.2
通讯作者：
MOEHRING, J
中科院分区：
文献类型：
--
作者：
BAKER, L;PIDDINGTON, R;MOEHRING, J
糖尿病母亲的婴儿神经管缺陷是导致新生儿死亡/发病和长期慢性残疾的一个重要而常见的原因。正常的神经管融合发生的机制尚不清楚。在过量D-葡萄糖存在下孵育的小鼠胚胎中出现的吻端神经管融合失败可以通过在培养液中添加肌醇来显著防止。肌醇的这种保护作用可被吲哚美辛逆转，吲哚美辛是导致前列腺素合成的花生四烯酸代谢的抑制剂。在培养液中加入前列腺素E_2可完全保护葡萄糖诱导的神经管缺陷。这些数据表明，糖尿病胚胎病变中神经管融合失败的机制涉及肌醇和花生四烯酸途径的异常，导致在神经管融合的关键时刻前列腺素功能不足。
Neural tube defects in infants of diabetics mothers constitute an important and frequent cause of neonatal motality/morbidity and long-term chronic handicaps. The mechanism by which normal neural tube fusion occurs is not known. The failure of rostral neural tube fusion seen in mouse embryos incubated in the presence of excess-D-glucose can be significantly prevented by the supplementation of myo-inositol to the culture medium. This protective effect of myo-inositol is reversed by indomethacin, an inhibitor of arachidonic acid metabolism leading to prostaglandin synthesis. Prostaglandin E2 added to the culture medium completely protects against the glucose-induced neural tube defect. These data suggest that the failure of neural tube fusion seen in diabetic embryopathy is mediated through a mechanism involving abnormalities in both the myo-inositol and arachidonic acid pathways, resulting in a functional deficiency of prostaglandins at a critical time of neural tube fusion.