摘要
[目的 ]通过对慢性铝接触大鼠不同脑区bcl 2基因表达水平的检测 ,研究神经细胞凋亡在铝中毒引起的学习记忆障碍中的作用。 [方法 ]给SD大鼠腹腔注射不同剂量的AlCl3 溶液 60d ,用跳台法测试其学习记忆能力的改变 ,用免疫组化法测定分析其脑组织不同脑区bcl 2基因表达水平。 [结果 ]与对照组相比 ,染铝组大鼠学习记忆能力明显下降 (P <0 0 5 ) ,大鼠跳台实验结果 ,潜伏期和 5min内错误次数明显增加 (P <0 0 5 )。大脑皮层和小脑各个剂量组bcl 2的表达都升高 (P <0 0 1) ,海马CA3区仅在中剂量组表达升高 (P <0 0 1)。 [结论 ]慢性铝接触可导致大鼠学习记忆障碍 ,出现类AD病人的早老性痴呆样症状 ,bcl 2基因作为重要的神经细胞凋亡抑制基因参与了这一毒性损害过程 ,并在其中起一定的保护作用 ;大脑皮质、海马及小脑部位的大量神经细胞凋亡很可能是铝毒性作用的重要机制之一。
To study the role of neuron apoptosis on the impairment of learning and memory induced by aluminum by detecting the expression of bcl 2 gene in different regions of chronic Al exposed rat brain. SD rats were exposed to aluminum by intraperitoneal injection of AlCl 3 solution for 60 days at different dose. The step down test was performed to test the learning and memory abilities in rats,and the expression of bcl 2 gene in neurons from different regions of rat brain was measured respectively using immuno histochemical method. Compared with the control group,the learning and memory abilities in the rats exposed to Al were obviously damaged ( P <0 05),the bcl 2 gene expression was upregulated in frontal cortex,CA3 area of hippocampus and cerebellum ( P <0 01),but necrosis of neurons was more evident in these parts of brain. [Conclusion] Chronic exposure to Al can cause the impairment of learning and memory in SD rats,following the AD like symptoms. Bcl 2 gene involved in causing these impairment and played a protective role as a suppressor gene of neuron apoptosis. A lot of necrotic neurons in different regions of brain may be one of the important intoxication mechanisms.
出处
《环境与职业医学》
CAS
北大核心
2002年第4期209-212,共4页
Journal of Environmental and Occupational Medicine
