【摘要】 目的构建D-半乳糖(D-galactose,D-ga)l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.方法大鼠腹腔注射D-gal100mg/(kg.d)×56d造模.第50～56天进行Morris水迷宫实验(MWM);第57天取脑组织,生物化学方法分光光度法检测大脑海马一氧化氮合酶(NOS)、一氧化氮(NO)、铜锌-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(H2O)2的表达水平.结果模型大鼠较正常大鼠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),海马内MDA、H2O2和NO表达增加,SOD、GSH、GSH-ST、GSH-Px、T-AOC表达降低,而NOS表达没有明显变化(P>0.05).结论D-gal能通过调控内源性巯基抗氧化物(酶),减退学习记忆能力,诱导大鼠神经系统的衰老.更多还原

【Abstract】 Objective To underlying investigate the mechanisms of the aging induced by D-galactose,we used D-galactose to establish aging rat model.Methods Aging rats model were established by peritoneal injection of D-Galactose(100 mg/kg,56 days)into the rats.Then,we examined spatial memory with the morris water maze,and the extent of oxidative stress biomarkers including malondialdehyde(MDA),total antioxidative capabilities(T-AOC),total superoxide dismutase(T-SOD),and glutathione peroxidase(GSH-Px)activities in hippocampus.Results Chronic systemic exposure of D-galactose to rats induced a spatial memory deficit and increased cerebral oxidative stress,including an increase in malondialdehyde(MDA),hydrogen peroxide(H2O2),nitric oxide(NO),while a decrease in total anti-oxidative capabilities(T-AOC),total superoxide dismutase(T-SOD),glutathione(GSH),glutathione peroxidase(GSH-Px),glutathione-s-transferase(GSH-ST)activities.Conclusion The present results suggest that chronic D-galactose exposure can induce a spatial memory deficit and aging of central nervous system by manipulating thiol antioxidants and NO of the hippocampus in rats.更多还原