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中文摘要：
目的探讨糖基化终末产物（AGEs）在β-淀粉样蛋白（Ap）产生中分子机制。方法以APPsw—N2a细胞为AD细胞模型，将细胞随机分为3组，空白对照组、AGEs组、AGEs＋抗RAG抗体组。采用ELIsA方法检测各组Aβ40和Aβ42的表达水平，并用荧光检测法检测BACE1的活性。结果与对照组相比，AGEs组AD40、Aβ42表达水平及BACE1活性明显增加，差异有统计学意义（P〈0．01）；预先用抗RAG中和抗体（1：100）1h后，A840，Aβ2表达水平及BACE1活性与AGEs组相比较明显减少，差异有统计学意义（P〈O．05）。结论AGEs可能通过上调BACEl的活性促使APPsw—N2a细胞A8生成增加，提示AGEs可能在AD发生、发展中起重要作用。
英文摘要：
Objective To investigate molecular mechanism of advanced glycation end products （AGEs） in the generation of β-amyloid protein（Aβ）. Methods The APPsw--N2a cells were divided into three groups randomly（the control group, the AGEs graup, the AGEs＋RAG group）. To examine the ceils＇ growth state with MTT metabolic rate and determine the best concentration and time of the AGEs, and to observe the generation of Aβ by ELISA. Results Our data showed that APP was up-- reg-ulated by AGEs in vitro, and pretreatment of cells with an anti--RAG--antibody blocked the effects of AGEs. In conditioned medium, the level of Aβ increased after AGE treatment. Conclusions AGEs could promote the generation of Aβ by up--regulating the activities of BACE.
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