磷酸化的JNK和p38在高温致神经管畸形上皮细胞中的表达变化

目的 探讨高温致神经管畸形（neural tube defects,NTD）的分子机制,为防治神经管畸形提供理论依据.方法 利用高温致金黄地鼠NTD动物模型,应用免疫荧光染色技术,观察NTD发生过程中磷酸化c-Jun氨基末端活化蛋白激酶（p-JNK）和磷酸化p38（p-p38）在胚胎神经管上皮的表达变化.结果 p-JNK和p-p38的免疫阳性产物表达于胚胎神经管上皮细胞及其周围间充质细胞的胞浆中,高温后不同时间点胚胎神经管上皮细胞内的p-JNK和p-p38的表达量均较对照组减弱.结论 磷酸化JNK和p38参与了神经管的正常发育,其表达量降低可能是高温致NTD发生的重要途径之一.

Expressional changes of phosphorylated JNK and p38 in neuroepithelial cells of neural tube defects induced by hyperthermia in golden hamsters

Objective To explore the molecular mechanism of neural tube defects （NTD） induced by hyperthermia, so as to provide a theoretical basis for the prevention of human NTD. Methods On the hyperthermia-induced golden hamster NTD model, the expressions of p-JNK and p-p38 in the neuroepithelial cells during the occurrence of NTD were detected using immunofluorescent staining. Results The results showed that p-JNK and p-p38 immunoreactivity was diffusely distributed in the cytoplasm of neuroepitheli- al cells and mesenchymal cells surrounded the neural tube. After maternal hyperthermia, the staining in- tensity of p-JNK and p-p38 immunoreactivity in the neuroepithelia of each experimental group was weaker than that of the control group. Conclusion The expressional changes of JNK and p38 are closely linked to the development of the neural tube, and the decreased expression of p-JNK and p-p38 may be one of the important ways for hynerthermia-induced NTD.