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中文摘要：
目的探讨阿尔茨海默病（AD）的发生、发展与神经细胞凋亡之间的规律,以及核转录因子κB（NF-κB）在神经细胞凋亡中的调节作用,为阿尔茨海默病的发病机理和临床治疗提供依据。方法分别取P0、P7、P14、P30、P90、P180日龄的APPSWE转基因小鼠为模型组,各日龄同窝生野生型小鼠为对照组,应用Nissl染色观察其海马结构和锥体细胞形态,免疫组织化学方法检测小鼠海马细胞内半胱天冬氨酸蛋白3（Caspase-3）表达及NF-κB激活情况,RT-PCR检测小鼠海马caspase-3 mRNA的表达。结果模型组及对照组小鼠海马CA3区锥体细胞中凋亡细胞密度和NF-κB阳性细胞密度均随日龄的增大而逐渐下降,在P30后趋于稳定;与对照组相比,模型组凋亡细胞密度和NF-κB阳性细胞密度均增高,自P14以后具有统计学意义（P〈0.01或P〈0.05）;RT-PCR检测小鼠海马caspase-3 mRNA表达结果与Caspase-3免疫组织化学检测结果基本吻合。结论凋亡相关基因caspase-3和NF-κB在阿尔茨海默病的发病机理中起重要作用,NF-κB的激活可能促进神经细胞凋亡。
英文摘要：
Objective To investigate the roles between the neuroapoptosis and the onset, development of Alzheimer＇ s disease, and the NF-κB＇ s regulation in neuroapoptosis. Methods APPSWE transgenic mice from postnatal day 0 to postnatal day 180 were used for Nissl staining, Caspase-3 and NF-κB immunohistochemistry and RT-PCR analysis. Results The neuroapoptosis and NF-κB immunostaining in CA3 areas decreased gradually with age increasing. In the meantime, the Caspase-3 positive pyramidal cells and NF-κB positive pyramidal cells were measured. The densities of both Caspase-3 and NF-κB positive cells in APPSWE transgenic mice were higher than that of the age-matched controls, and there were statistical differences after P14 （P 〈 0.01 or P 〈 0. 05）. In addition, the result of RT-PCR was coincident with that of immunohistochemistry. Conclusion The onset and development of Alzheimer＇ s disease may be relevant to apoptosis-related genes, Caspase-3 and NF-κB. The action of NF-κB may activate the Caspase-3 expression and neuroapoptosis.
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