中文摘要：

调查亚 chronic Aluminium-maltolate 的影响的目的[艾尔(mal ) 3 ] 在老鼠的淀粉的先锋蛋白质(应用软件) 的分解代谢上的暴露。四十只成年男 Sprague-Dawley (SD ) 老鼠随机被划分成五个组的方法：控制组， maltolate 组(7.56 mg/kg BW ) ，和 3 组织的艾尔(mal )(0.27， 0.54，和 1.08 mg/kg BW，分别地) 。控制老鼠与通过 intraperitoneal (i.p ) 盐的 0.9% 正常被管理注射。Maltolate 和艾尔(mal ) 3 通过 i.p 注射也予老鼠被以。管理每天被进行二个月。老鼠神经行为用田野测试被检验(经常) 。并且蛋白质表达式和他们与应用软件分解代谢联系的 mRNAs 抄写用连接酶的 immunosorbent 试金(ELISA ) 和即时聚合酶链反应(RT-PCR ) 被学习。应用软件，劈开酶 1 的地点应用软件(BACE1 ) 和 presenilin-1 (PS1 ) 蛋白质和他们的 mRNAs 抄写的表情随 3 开的艾尔(mal ) 的增加逐渐地增加了的结果(P < 0.05 ) 。在 3 组织的 0.54 和 1.08 mg/kg 艾尔(mal ) 的 BACE1 的酶活动显著地增加了(P < 0.05 ) 。淀粉的蛋白质(A) 的表示当 A142 的蛋白质表示随 3 开的艾尔(mal ) 的增加逐渐地增加了时， 140 逐渐地减少了(P < 0.05 ) 。从我们的学习的结论结果建议了 3 能引起 neurotoxicity 的艾尔(mal ) 是 3 能增加的那艾尔(mal ) 的一可能的机制由便于应用软件的表达式的 A142 的产生，，并且 -secretase。

英文摘要：

Objective To investigate the impact of sub-chronic Aluminium-maltolate [Al（mal）s] exposure on the catabolism of amyloid precursor protein （APP） in rats. Methods Forty adult male Sprague-Dawley （SD） rats were randomly divided into five groups： the control group, the maltolate group （7.56 mg/kg BW）, and the Al（mal）s groups （0.27, 0.54, and 1.08 mg/kg BW, respectively）. Control rats were administered with 0.9% normal saline through intraperitoneal （i.p.） injection. Maltolate and Al（mal）s were administered to the rats also through i.p. injections. Administration was conducted daily for two months. Rat neural behavior was examined using open field tests （OFT）. And the protein expressions and their mRNAs transcription related with APP catabolism were studied using enzyme-linked immunosorbent assay （ELISA） and real-time polymerase chain reaction （RT-PCR）. Results The expressions of APP, 13-site APP cleaving enzyme 1 （BACEI） and presenilin-1 （PSi） proteins and their mRNAs transcription increased gradually with the increase of Al（mal）3 doses （P〈0.05）. The enzyme activity of BACEI in the 0.54 and 1.08 mg/kg Al（mal）s groups increased significantly （P〈0.05）. The expression of 8-amyloid protein （AS） 1-40 gradually decreased while the protein expression of A81-42 increased gradually with the increase of Al（mal）s doses （P〈0.05）. Conclusion Result from our study suggested that one of the possible mechanisms that Al（mal）s can cause neurotoxicity is that Al（mal）s can increase the generation of A81-42 by facilitating the expressions of APP, β-, and γ-secretase.