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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。
Objective To investigate the protective effect of Glycosides of cisatan (GCs) on Alzheimer’s disease (AD) mice induced by β-amyloid peptide (β-AP) and to explore its mechanism of action. METHODS: Intracerebral intraventricular single-injection microinjection of β-AP25-35 induced beta-AP deposition in the brain, resulting in an AD mouse model. After 10 days, passive learning avoidance was used to determine the ability of learning and memory in AD mice; SOD activity, MDA content and GSH-Px activity in brain tissue were detected; pathological changes of neurons in brain tissue were detected by electron microscopy; The death; immunohistochemical SABC method to detect the expression of Bax/Bcl-2. Results GCs could improve the learning and memory of AD mice induced by β-AP; decrease the content of MDA in brain tissue, increase the activity of SOD and GSH-Px; improve some pathological changes in brain tissue; decrease the rate of apoptosis of brain cells; The expression decreased and the expression of Bcl-2 was increased. Conclusion GCs can improve the learning and memory ability of AD mice induced by β-amyloid peptide. The mechanism may be related to the enhancement of free radical scavenging enzyme activity, prevention of lipid peroxidation, inhibition of the deposition of β-AP in the brain and inhibition of brain cells. Apoptosis related.