中文摘要：

构建D-半乳糖（D-gal）致衰老模型，探讨D-gal诱导衰老的分子机制，为临床治疗阿尔茨海默病（AD）提供理论依据。腹腔注射D-gal构建SD大鼠衰老模型，采用Morris水迷宫实验（MwM）进行行为学检测，采用化学比色法检测大脑皮质一氧化氮合酶（NOS）、一氧化氮（NO）、铜锌一过氧化物岐化酶（Cu，Zn-SOD）、总超氧化物歧化酶（T-SOD）、谷胱甘肽还原酶（GR）、谷胱甘肽S-转移酶（GSH-ST）、谷胱甘肽过氧化酶（GSH-PX）、谷胱甘肽（GSH）、丙二醛（MDA），总抗氧化能力（T-AOC）和过氧化氢（H2O2）的含量。结果显示：衰老模型组与正常对照组比较：逃避潜伏期明显延长（P〈0．05），在第Ⅲ象限逗留的时间明显减少（P〈0．05），跨越平台次数明显减少（P〈0．05）；皮质MDA、H202和NO的含量增加（P〈0．05），SOD、GSH、GSH-ST、GSH-Px和T-AOC的含量降低（P〈0．05），而NOS的含量没有明显变化（P〉0．05）。结果提示，D-gal能通过调控内源性巯基抗氧化物（酶）和NO的表达，减退学习记忆能力，而诱导SD大鼠神经系统的衰老：

英文摘要：

To investigate the molecular mechanisms of the aging induced by D-galactose, we used D-galactose- aging rat model, so as to provide basic theory for treating Alzheimer＇s disease （AD） in clinic. Aging rat model was established by injecting peritoneally D-Galactose （ 100 mg/kg, 56 days） into the rats. The behaviour was examined by the Morris water maze （MWM）. The nitric oxide synthase （NOS） , nitric oxide （ NO）, Cu Zu-superoxide dismutase （ Cu Zn-SOD） , total superoxide dismutase （T-SOD） , glutathione reductase （GR） , Glu- tathione-s-transferase （ GSH-ST）, glutathione peroxidase（ GSH-Px）, glutathione （ GSH）, malondialdehyde （ MDA）, anti-oxidative capabilities （T-AOC） and hydrogen peroxide （H2 02 ） activities were examined by colorimetric method. The results showed that the model rats exhibited significant increase in escape latencies （ P 〈 0.05 ）, while a decrease in the time of staying in quadrant of platform and the num- ber of crossing over a platform as compared to control group （ P 〈0.05 ）. The cortex of the model rats showed significant increase in MDA, H2O2 and NO activities（P 〈 0.05）, while a decrease in T-AOC, T-SOD, GSH, GSH-Px and GSH-ST activities as compared to control group （ P 〈 0.05 ）. However, the difference of NOS activity was not detected between two groups （ P 〉 0.05 ）. These present results suggest that Chronic D-galactose exposure can injure the spatial memory and induce the aging of central nervous system by manipulating thiol an- tioxidants and NO of the cerebral cortex in SD rats.