目的 探讨孕期酒精接触对子鼠视皮质神经元凋亡的影响。方法 从妊娠母鼠第5d酒精灌胃直至小鼠出生;采用激活的半胱氨酸天冬氨酸蛋白3(Caspase-3)免疫组织化学和原位末端标记(TUNEL)法观察P0、P7和P14小鼠视皮质神经元的凋亡。结果 酒精实验组妊娠时间延长,出现死胎和畸形(小头畸形、无脑儿和脊柱脊髓裂等)。酒精实验组Caspase-3阳性率和凋亡指数明显高于对照组(P〈0.001)。高剂量酒精组明显高于低剂量组(P〈0.01)。随着酒精剂量的增加。子鼠视皮质神经元的凋亡明显增加。结论 孕期酒精接触可导致子鼠视皮质神经元凋亡,且有剂量依赖性和长时程效应。
Objective To study ethanol-induced the neuroapoptosis of visual cortex in offspring mice. Methods Pregnant female mice were fed by intubatlng alcohol daily, beginning on E5 (embryonic, E) and continuing through the pup' s birth. The neuroapoptasis in P0, P7 and PI4 visual cortex was visualized by Caspase-3 activity immunohistochemistry and Terminal deoxynucleotidyl transferase biotin-dUTP nick end labeling (TUNEL) staining. Results Usually, the pup's birth days would delay one or two days after ethanol exposure. Moreover, ethanol induced reabsorption of fetus and malformations, such as microcephaly, anencephaly and myeloschisis with spinabifida and so on, were found in the study. Apoptosis index in ethanol treatment groups was obviously higher than that in control at either P0, P7 or P14 (P 〈 0.001 ). In the meantime, high ethanol dose group had a higher apoptosis index than that of low dose ethanol group ( P 〈 0.01 ). Conclusion The prenatal ethanol exposure could induce neuroapoptosis of visual cortex with dose-dependency and long-term effects.