中文摘要：

目的研究β淀粉样蛋白（Aβ1-42）对原代培养基底前脑胆碱能神经元ATP敏感性钾通道（KATP）各亚基蛋白表达的影响,探讨阿尔茨海默病发病的细胞毒性分子机制。方法运用细胞原代培养的方法培养大鼠基底前脑胆碱能神经元并进行鉴定,用2μmmol/L的Aβ1-42对原代培养细胞进行干预,免疫荧光双染及免疫印记观察干预后不同时间（分别为0,24,72 h）细胞KATP通道各亚基Kir6.1、Kir6.2和SUR1、SUR2蛋白表达水平的变化。结果与正常对照组比较,Aβ1-42作用胆碱能神经元24 h后,KATP通道亚基Kir6.1及SUR2蛋白表达显著增多（P〈0.05）,而亚基Kir6.2及SUR1蛋白表达无明显变化。但Aβ1-42作用时间达72 h后,KATP通道各个亚基蛋白表达均显著升高（P〈0.05）。结论Aβ1-42作用胆碱能神经元不同的时间段（24 h和72 h）,细胞KATP通道各亚基蛋白表达有不同程度的增加,且增加速度不一致。可能由此改变KATP通道的结构和功能,从而影响Aβ1-42的神经细胞毒性作用。

英文摘要：

Objective To investigate the effects of Beta-amyloid peptides （Aβ1-42） on the subunits of KATp expression of cultured primitive basal forebrain cholinergic neurons in rats. Methods Primitive rat basal forebrain neurons were cultured and evaluated. The subunits of KATP ： Kir6.1, Kir6.2, SUR1 and SUR2 expression were determined by double immunofluorescence and immunoblotting when the neurons were exposed to Aβ1-42 （2 μmol/L） for different times （0, 24 and 72 h）. Results After being exposed to Aβ1-42 for 24 hours, the expression of subunits Kir6.1 and SUR2 in the cultured neurons was significantly increased compared with the controls （ P 〈 0.05）, while that of Kir6.2 and SUR1 had no significant difference from that of the controls. After being exposed to Aβ1-42 for 72 hours, the expressions of the four subunits were all significantly increased compared with the controls （ P 〈 0.05）. Conclusion Aβ1-42 for different times （24 h and 72 h） induces different regulation of KATP subunit expressions in cultured primitive rat basal forebrain cholinergic neurons. Changes in composition of KATP may resist the toxicity of Aβ1-42