中文摘要：

目的 通过研究Bcl-2和Bax蛋白及基因在铝致神经细胞毒性作用中的表达,以探讨铝对体外培养大鼠神经元细胞的神经毒性作用.方法 用不同浓度氯化铝体外培养大鼠神经元细胞染毒,用原位缺口末端标记（TUNEL）法和扫描电镜观察检测细胞凋亡,免疫组化法测定Bcl-2和Bax蛋白含量,RT-PCR法测定Bcl-2和Bax基因表达量.结果 （1）TUNEL法检测DNA碎片随染铝剂量的加大而增加,扫描电镜观察到了凋亡细胞典型的出芽现象和细胞裂解及凋亡小体的释放.（2）免疫组化和RT-PCR法检测Bcl-2蛋白含量及基因表达量随染铝剂量的加大而减少（P＜0.01,r=-0.695;P＜0.05,r=-0.647）,反之,Bax蛋白含量及基因表达量随染铝剂量的加大而增加（P＜0.01,r=0.676;P＜0.01,r=0.794）.Bcl-2/Bax与铝的作用剂量有关（P＜0.01,r=-0.655;P＜0.01,r=-0.777）.结论 低剂量铝暴露能够诱导神经元凋亡,Bcl-2和Bax蛋白及基因表达在铝致神经细胞凋亡的过程中发挥了重要的调控作用.

英文摘要：

Objective To study the role of Bcl-2 and Bax protein contents and their gene expression in Al-induced neurons apoptosis. Methods Neurons from 0-3 day rats were cultured and treated with different concentrations of AlCl3·6H2O. The cell apoptosis was observed by the TUNEL method and under the scan electron micrescope. Bcl-2 and Bax protein contents were detected by the immunochemistry method while their gene expressions were measured by the RT-PCR method. Results （ 1 ）DNA fractions in the TUNEL method increased with the rising aluminum concentration. Blebbings and apoptosis bodies on the surface of the neurons were clearly observed under the scan electron microscope. （2）Bcl-2 protein contents and their gene expression decreased with the rising aluminum concentration（ P 〈 0.01, r = - 0. 695 ; P 〈 0.05, r = - 0. 647）, while Bax increased at the same time （ P 〈 0.01, r = 0.676; P 〈 0.01, r = 0.794）, the value of Bcl-2/Bax was related with the aluminum concentration （P〈0.01,r= -0.655;P〈0.01,r= -0.777）. Conclusion The aluminum may induce neurons apoptosis. Bcl-2 and Bax protein contents and their gene expression may play an important role in Al-induced apoptosis.