摘要
目的:观察不同孕期补碘所引起的高碘对子鼠脑凋亡及调节基因表达的影响情况。方法:受精大鼠分成3个组,2个高碘组分别在受孕0 d和7 d一次性经口灌胃给予1 ml/kg.bw 40%碘化油、对照组给予同剂量食用豆油。用免疫组化法测定21、28、35 d龄子鼠海马bc1-2、bax蛋白表达;TUNEL法测定35 d龄子鼠神经元细胞凋亡状况。结果:与对照组比较,在海马各亚区,两个高碘组bcl-2蛋白表达减少,bax蛋白表达增多;高碘Ⅰ组凋亡指数增高,高碘Ⅱ组指数虽增高但无统计学意义。结论:孕期补碘性高碘可使子鼠海马神经细胞凋亡增加,作为凋亡调控基因bcl-2、bax可能参与了高碘诱导海马神经元凋亡的过程。
Objective： To observe the effect of excess iodine caused by supplying iodine during different gestation period on the neuron apoptosis and gene expression of filial rats. Methods： Fertilized rats were divided into three groups, 40% iodide oil was injected into two high iodine group＇ s stomach through mouth with 1ml/kg.bw at day 0 and day 7 respectively. At the same time, edible bean oil was injected into control group by the same way. For PN21, PN28、 PN35 offspring, the expressions of bcl-2 and bax gene were measured by immunohistochemistry. For PN35 offspring, the neuron apoptosis were examined by TUNEL. Results： Compared with control group, in hippocampus CA1, CA3, IX; region, the expression intensity of bel- 2 of high iodine group decreased, but expression intensity of bax increased; the apoptosis index of the first group increased, although the second group was higher than control group, but there was no statistical significance. Conclusion： Excess iodine caused by supplying iodine daring gestation can cause hippocampus neuron apoptosis increase of the filial rats. As a regulative and control gene of PCD, bcl - 2 arid bax may participate in this process.
出处
《现代预防医学》
CAS
北大核心
2006年第12期2225-2226,2230,共3页
Modern Preventive Medicine
基金
国家科技部"十五"科技计划项目(2001BA901A49)
