高温致神经管畸形中bcl-2和bax变化的动物实验研究

Experimental Studies of bcl-2 and bax in Neural Tube Deffects Induced by Hyperthermia

目的 探讨高温致神经管畸形的分子机制。方法 在高温致金黄地鼠神经管畸形的动物模型上 ,利用免疫组织化学法 (SABC法 )染色 ,观察神经管畸形发生过程中凋亡相关基因bcl 2和bax在神经上皮细胞中的表达变化。结果 高温后 8h开始 ,实验组鼠胚神经上皮细胞bcl 2的表达均不同程度低于对照组 ,尤以高温后 16h差异最为显著 ,2 4h后实验组与对照组相比bcl 2的表达差异无显著性。高温后 8h ,16h ,实验组鼠胚神经上皮细胞bax的表达均明显高于对照组 ,2 4h后实验组与对照组相比bax的表达差异无显著性。结论 高温抑制bcl 2的表达 ,促进bax的表达 ,诱发神经上皮细胞的凋亡 。

Objective To explore the molecular mechanism of neural tube defects (NTDs) induced by hyperthermia.Methods On the hamster NTDs model in vivo,expressions of bcl 2 and bax in the neuroepithelial cells were examined with immunohistochemistry.Results After 8 hour exposure,the level of bcl 2 in the neuroepithelia was lower than control group,most obvious at the 16th hour,then returned to control level by 24 hours.Meanwhile the amount of bax was significantly higher than the control groups at 8 hour and 16 hour.After 24 hours,the level of bax was near the control level.Conclusion Hyperthermia may suppress the expression of bcl 2 gene,otherwise promote the bax gene expression during development,result in excessive apoptosis in neuroepithelia,thereby inducing development of neural tube defects.