摘要
目的探究荭草苷对APP/PS1转基因小鼠认知功能的影响及其可能的作用机制。方法实验动物分为3组:7月龄的转基因模型组(Tg)、荭草苷处理转基因组(Tg+Ori)、同月龄的野生型C57BL/6J小鼠作为非转基因对照组(NT),每组8只。Tg+Ori组连续30 d每天腹腔注射荭草苷(10 mg·kg^(-1)),NT和Tg组注射同等剂量的生理盐水。水迷宫实验检测学习记忆能力,免疫组化检测β淀粉样蛋白(Aβ),免疫印迹检测自噬相关蛋白。结果与NT组相比,Tg组小鼠学习记忆能力受损,海马出现大量Aβ斑块, LC3-Ⅱ、p62、Cathepsin D蛋白表达升高;与Tg组相比,Tg+Ori组小鼠学习记忆能力增强,海马Aβ斑块减少,LC3-Ⅱ、p6、Cathepsin D蛋白水平降低;组间Beclin-1蛋白水平无明显差异。结论荭草苷能够改善转基因小鼠认知功能,减少海马Aβ沉积,促进自噬溶酶体降解。
Aim To study the influence of orientin on the cognitive function in APP/PS1 double transgenic mice and the probable mechanisms. Methods The mice (7 months of age) were randomly assigned into three groups ( n =8 in each group): non-transgenic mice (NT) and APP/PS1 transgenic mice (Tg) were given saline,and APP/PS1 transgenic mice with orientin (Tg+Ori),and were injected intraperitoneally once per day for 30 days.Morris water maze test was carried out for the evaluation of spatial learning and memory.The measurement of Aβ was conducted by immunohistochemical staining.Autophagy related protein expressions of LC3-Ⅱ,p62,Cathepsin D and Beclin-1 were measured by Western blot. Results Compared with NT group,Tg mice showed deficit memory formation,enhanced Aβ deposition and protein levels of LC3-Ⅱ,p62 and Cathepsin D;compared with Tg group,Tg+Ori mice showed improved learning and memory,reduced Aβ load,and decreased levels of LC3-Ⅱ,p62 and Cathepsin D.The expression of Beclin-1 showed no difference between groups. Conclusions Orientin could improve the cognitive function,reduce amyloid plaques and ameliorate hippocampus autophagic clearance of APP/PS1 transgenic mice.
作者
钟轶
郑晴予
贾宁
孙承艳
韩锟
ZHONG Yi;ZHENG Qing-yu;JIA Ning;SUN Cheng-yan;HAN Kun(Dept of Neurology,the First Affiliated Hospital of Jinzhou Medical University,Jinzhou Liaoning121001,China;Dept of Anatomy,Foundation Institute of Jinzhou Medical University,Jinzhou Liaoning121001,China)
出处
《中国药理学通报》
CAS
CSCD
北大核心
2019年第5期686-690,共5页
Chinese Pharmacological Bulletin
基金
辽宁省科技厅博士启动基金(No 201601357)
关键词
阿尔茨海默病
荭草苷
认知功能
海马
自噬
淀粉样Β蛋白
Alzheimer’s disease
orientin
cognitive function
hippocampus
autophagy
amyloid beta-peptides
