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【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 investigate the molecular mechanism of oyster antagonism of neuronal apoptosis in neural tube defects (NTDs) caused by retinoic acid (RA). 【Methods】 NTDs models were established and the oyster was antagonized. The apoptosis of neurons and the expression of Bcl-2, Bax and Caspase-3 were observed. 【Results】 1) The apoptosis index of neural tube epithelial cells in RA group was significantly higher than that in control group, and the apoptosis index in oyster group was significantly lower than that in RA group (P <0.05). 2) The expression of Bcl-2 in RA group was significantly lower than that in control group. The expression of Bcl-2 in oyster group was significantly higher than that in RA group (P <0.05). 3) The expressions of Bax and Caspase-3 in RA group were significantly higher than those in control group, while the expression of Bax and Caspase-3 in oyster group was significantly lower than that in RA group (P <0.05). 【Conclusion】 Oyster can antagonize RA-induced excessive apoptosis of neuroepithelial cells by up-regulating Bcl-2 expression and down-regulating Bax and Caspase-3 expression.