高铝致老龄大鼠痴呆及其原理初探

目的 探讨高铝与老龄大鼠痴呆的关系及原理。方法 实验前用花生米和节拍器建立大鼠条件反射。再用含铝和铝加柠檬酸的溶液饲养大鼠4个月，从条件反射恢复的时间和数量反映各组大鼠痴呆发病率，测定血液中铝和MDA含量，测定脑中铝合量和海马区细胞凋亡指数，其凋亡指数以平均光密度值(OD)表示。结果 实验二组与一组相比，铝、MDA及OD值增加，条件反射恢复，数量减少，两组间有显著性差异P＜0．01。实验三组与二组相比，铝、MDA、OD值增加，条件反射恢复，数量进一步减少，与二组相比均有显著性差异P＜0．01。结论 柠檬酸能增加机体对铝的吸收，使体内铝进一步增加，高铝能促进铝在脑细胞内的沉积，促进体内MDA生成和脑细胞的凋亡，因而增加大鼠痴呆发生率。

A Primary Study on the Aging Rats Dementia Induced by High Aluminum and its Mechanism

Objective To investigate the relationship between the high Aluminum and the aging rat dementia and explore its mechanism.Methods The conditioned reflex was established among all the aging rats by using peanut and ting before experiment.Then the rats were divided into three groups:the control group,the Al group,and the Al+citric acid (Cit) group.The Al group and the Al+Cit group had been fed with the water containing high Aluminium (the Al group)or high aluminium plus citric acid for 4 months.Thereafter,the conditioned reflex was established again in all the groups.The morbidity of the aging rat dementia was expressed by the time of the recovery from the conditioned reflex and the number of the rats whose conditioned refex recovererd.The serum aluminium level,MDA level and the aluminium content in brain were measured.The apoptotic index was expressed by the mean optical density value (OD value) from the sections.Results Compared with group one,the Al group showed the increase in Aluminium content,MDA level and OD value,but the number of the rats whose conditioned reflex recovered decreased in the Al group.The difference between the two group was significant (P<0.01).The Al+Cit group showed a rise of the Al content,MDA level,apoptotic index and OD value than those of group two,but the number of the rats whose conditioned reflex recovered decreased.The difference between the two groups was marked(P<0.01).Conclusion Citric acid can stimulate the absorption of alumunium, thus induce the rise in the aluminium contents in body.The high aluminium can deposit into the brain cell ,stimulate the production of MAD and apoptosis in the brain, and thereafter increase the morbidity of the aging rat dementia.