肉苁蓉总苷对β-淀粉样肽所致阿尔采末病小鼠模型学习记忆的影响及其机制

目的研究肉苁蓉总苷(G lycosides of c istanche,GCs)对β-淀粉样肽(β-AP)所致阿尔采末病(AD)模型小鼠的保护作用,并探讨其作用机制。方法采用小鼠脑室内一次性微量注射β-AP25-35诱发β-AP在脑内的沉积,造成AD小鼠模型。10 d后,一次性训练被动回避跳台实验测定AD小鼠学习记忆能力;检测脑组织SOD活性、MDA含量及GSH-Px活性;电子显微镜检测脑组织神经细胞的病理变化;TUNEL法检测脑细胞凋亡;免疫组化SABC法检测Bax/Bc l-2的表达。结果GCs可提高β-AP所致AD小鼠学习记忆水平;降低脑组织MDA含量,提高SOD及GSH-Px活性;使脑组织中某些病理改变得到改善;降低脑细胞凋亡率;使Bax的表达减弱,Bc l-2的表达增强。结论GCs对β-淀粉样肽所致AD小鼠学习记忆能力提高,其作用机制可能与其增强自由基清除酶活性,防止脂质过氧化作用,抑制β-AP在脑内的沉积及抑制脑细胞凋亡有关。

The effects of glycosides of cistanche on learning and memory in β-amyloid peptide induced Alzheimers disease in mice and its possible mechanism

Aim To study the protective effects of gly-cosides cistanche(GCs) on model of Alzheimers dis-ease(AD) in mice induced by β-amyloid peptide(β-AP) and its mechanism.Methods AD animal model was established by a single intracerebroventricular injection of micromolar doses of β-AP_(25-35) in mice.After 10 days,a step-through type passive avoidance training was performed on the mice for one time,followed by a ability assessment of learning and memory;superoxidase dismutase(SOD) activities,gultathionine peroxides(GSH-Px) activities and malondialdehyde(MDA) contents in mice brain were also assessed;the pathological changes in the AD mice brain were observed by electronic microscopy;TUNEL method was used to observe the apoptosis of cells;the immunohistochemical SABC method was used to determine expression of Bcl-2 and Bax.Results GCs markedly enhanced the ability of learning and memory which induce by β-AP in AD mice and increased the activity of SOD and GSH-Px,and reduced MDA contents in mice brain;GCs also ameliorated some pathological features of AD mice brain and significantly decreased cell apoptosis in mice brain.A decrease in the Bax expression and a increase in the Bcl-2 expression were also observed.Conclusions GCs significantly improves the ability of learning and memory induced by β-AP in AD mice and its possible mechanism of action may involve: Enhancement of free radical scavengers;inhibition of lipid peroxidation;inhibition of β-AP precipitation and apoptosis in mice brain cells induced by β-AP.