宫内及哺乳期铅接触子鼠海马神经元凋亡及bcl-2、bax基因的表达  

The effects of lead exposure during intrauterine and lactation in filial rats on neuron apoptosis and the expressions of bcl-2 and bax in hippocampus formation

作　　者：雷荣辉[1] 张进[1] 易建华[1] 苗江丽[1] 席小平[1] 张敬华[1] 

机构地区：[1]西安交通大学医学院劳动卫生与卫生毒理学教研室,西安710061

出　　处：《西安交通大学学报（医学版）》2003年第1期27-29,共3页Journal of Xi’an Jiaotong University（Medical Sciences）

基　　金：国家教委高等教育行动计划资助项目 (No:X160 0 82 0 0 3)

摘　　要：目的　探讨宫内及哺乳期铅接触对子鼠海马神经元凋亡的诱发作用及对bcl 2、bax基因表达的影响。方法　SD大鼠采用饮水加 2 0 0 0mg·L-1醋酸铅染毒 6周后 ,雌雄按 2∶1合笼 ,自然分娩 ,于子鼠断乳时停止染毒 ,用原位末端标记TUNEL法检测海马神经元的凋亡状况 ;用SP免疫组化法观察凋亡调控基因bcl 2、bax表达。结果　TUNEL法染色结果显示 :染铅组子鼠海马CA1、CA3、齿状回 (DG)区神经元细胞凋亡指数均明显高于对照组 ,差异有显著性 (P <0 .0 1) ;SP免疫组化结果显示 :染铅组子鼠海马CA1、CA3、DG区bcl 2阳性细胞数表达较对照组减少 ,而bax阳性细胞数表达较对照组增多。结论　宫内和哺乳期铅接触可导致子鼠海马神经元凋亡 ,其机制可能与海马bcl 2蛋白表达下降。Objective To explore the effects of lead exposure during intrauterine and lactation in filial rats on neuron apoptosis and the expressions of bcl-2 and bax genes in hippocampus formation and the relationship between them. Methods SD rats were exposed to 2?000?mg·L -1 of lead acetate in their drinking water for 6 weeks, and then mated. Their offsprings were exposed to lead only during intrauterine and lactation. At postnatal day 21(PN21d), the neuron apoptosis was examined with terminal deoxynucleotidyl transferase mediated dUTP biotined nicked end labeling (TUNEL) in the different hippocampal subareas. The expressions of the bcl-2 and bax gene were examined with SP immuno-histochemistry. Results The indices of neuron apoptosis in CA1,CA3 and DG regions of lead-exposed offsprings were significantly higher than those of control(P<0.01). The expression of bcl-2 of lead-exposed offsprings was significantly lower than those of control, and the expression of bax of the lead-exposed was significantly higher than that of control. Conclusions Lead may cause neuron apoptosis in the hippocampus through the down regulation of bcl-2 gene expression and the up regulation of bax expression.

关 键 词：铅 海马 凋亡 bcl-2 BAX 

分 类 号：R995[医药卫生—毒理学]