目的:研究孕期酒精暴露对子鼠海马神经元凋亡的影响。方法:采用健康C57BL/6J小鼠,用胃饲酒精法建立孕期酒精暴露模型。90只孕鼠随机分为3组:对照组、低剂量酒精组和高剂量酒精组。低、高剂量酒精组分别按2.0g/kg与4.0g/kg的剂量给予体积分数为25%的乙醇,1次/d,直至子鼠出生,对照组自由饮食。3组取新生鼠、生后7d与生后14d的小鼠各10只,取海马组织进行caspase-3免疫组化染色,以观察海马神经元的凋亡。结果:低剂量酒精组和高剂量酒精组各年龄子鼠海马神经元caspase-3阳性率明显高于对照组(P〈0.01);高剂量酒精组海马神经元caspase-3阳性率明显高于低剂量酒精组(P〈0.01)。结论:孕期酒精暴露可激活发育期海马神经元caspase-3,诱发神经元凋亡,可能与出生子鼠智力障碍密切相关。
Aim : To investigate the effects of alcohol exposure during pregnancy on neuroapoptosis of hippocampus in filial mice. Methods: Clean-grade C57BL/6J mice were used. The pregnant mice were randomly divided into 3 groups: control group, low-dose alcohol group and high-dose alcohol group. Mice in low or high-dose alcohol groups received 25% ethanol by gavage at a dose of 2.0 g/kg and 4.0 g/kg, respectively, 9nce per day, till the pup's birth, and the control group were allowed free access to food and water. Caspase-3 staining was performed in hippocampus in neonatal, 7-day old and 14-day old mice from the 3 groups to detect neuronal apoptosis. Results: The caspase-3 positive rate in low-dose alcohol group and high-dose alcohol group was obviously higher than that in control group (P 〈 0. 01 ) , and the caspase-3 positive rate in high-dose alcohol group was higher than that in low-dose alcohol group(P 〈0.01 ). Conclusion: The prenatal alcohol exposure can activate caspase-3 and induce neuronal apoptosis in the developing hippocampus of mice, which may be closely related to low intelligence of filial mice.