目的 探讨维甲酸(retinoic acid,RA)致神经管畸形(neural tube defects,NTDs)中牡蛎拮抗神经细胞凋亡的分子机制。方法 建立NTDs模型并给予牡蛎拮抗,观察神经细胞的凋亡情况及凋亡相关蛋白Bcl-2、Bax与Caspase-3表达的变化。结果 1)RA组神经管上皮细胞凋亡指数明显高于对照组,牡蛎组凋亡指数明显低于RA组(P＜0.05)。2)RA组神经上皮细胞Bcl-2的表达明显低于对照组,牡蛎组Bcl-2的表达明显高于RA组(P＜0.05)。3)RA组Bax与Caspase-3的表达均明显高于对照组,牡蛎组Bax与Caspase-3的表达明显低于RA组(P＜0.05)。 结论 牡蛎可以拮抗RA引起的神经上皮细胞过度凋亡,其机理可能是通过上调Bcl-2的表达和下调Bax与Caspase-3的表达实现的。

Objective To explore the molecular mechanism of oyster antagonistic neuronal apoptosis in neural tube defects(NTDs) caused by retinoic acid(RA). Methods NTDs model was set up in mouse embryo by overdose RA and was given the antagonists of oyster.The apoptosis situation and expression changes of apoptosis related proteins Bcl-2,Bax and Caspase-3 in neural epithelial cells of mouse embryo were observed. Results 1)The apoptotic index of neuroepithelial cells in RA group was significantly higher than that in the control group(P＜0.05).The apoptotic index of neuroepithelial cells in oyster group was significantly lower than that in RA group(P＜0.05).2)Bcl-2 expression of neuroepithelial cells in RA group was significantly lower than that in the control group(P＜0.05).Bcl-2 expression in oyster group was significantly higher than that in the RA group(P＜0.05).3)Bax and Caspase-3 expression on neur epithelial cells in RA group were significantly higher than that in the control group(P＜0.05).Bax and Caspase-3 expression in oyster group was significantly lower than that in the RA group(P＜0.05). Conclusion Oysters can antagonize neur epithelial cells excessive apoptosis in NTDs caused by RA.Its molecular mechanism may be realized through the up-regulation of Bcl-2 expression and down-regulation of Bax and Caspase-3 expression.