氯化铝对大鼠脑组织胶质原酸性纤维蛋白和淀粉样β-蛋白前体基因表达的影响

Effects of aluminum chloride on amyloid β protein precursor and glial fibrillary acidic protein expression in rat cortex 1

为探讨铝和早老性痴呆（ＡＤ）及其他神经退行性疾病之间的关系及其作用机理，使用原子吸收，免疫组化和Ｎｏｒｔｈｅｒｎ印迹法等检测方法，观察饮用含铝饮水６个月的大鼠脑皮层中Ａｌ３＋和淀粉样β－蛋白前体（β－ＡＰＰ６９５）ｍＲＮＡ及皮层和海马区胶质原酸性纤维蛋白（ＧＦＡＰ）的含量变化．结果发现，ＡｌＣｌ３（７．４和１４．８ｍｍｏｌ·Ｌ－１）在引起脑皮层中铝的含量明显增高的同时，皮层和海马ＧＦＡＰ免疫组化阳性指数升高，皮层β－ＡＰＰ６９５ｍＲＮＡ的含量增加．在饮水铝浓度为１４．８ｍｍｏｌ·Ｌ－１时，β－ＡＰＰ６９５ｍＲＮＡ的相对含量是对照组的２．５倍．结果表明，长期铝接触可以引起胶质细胞增生和β－ＡＰＰ表达的改变．提示铝可能是ＡＤ等神经退行性疾患的一个致病或促发因素．

To explore the relation between aluminum and Alzheimer′s disease(AD) and other neurogenerative diseases, atom absorption spectrometry, immunohistochemistry and Northern blot assay were used to determine Al 3+ and amyloid β protein precursor(β APP) mRNA contents in cortex, glial fibrillary acidic protein(GFAP) antigen level in hippocampus and cortex of rats fed with AlCl 3 (7.4 and 14.8 mmol·L 1 ) in drinking water for 6 months. The results showed that the contents of Al 3+ and β APP mRNA in cortex, the immunohistochemical positive index of GFAP in hippocampus and cortex notably increased. β APP mRNA relative content at 14.8 mmol·L 1 was 2.5 times of that of controls. These results suggest that a long term exposure to aluminum result in a proliferation of astrocytes and abnormality of β APP gene expression, aluminum be one of the pathogenic or accelerating factors of AD and other neurogenerative diseases by inducing the overexpression of GFAP and β APP.