The seed of Litchi chinensis fraction ameliorates hippocampal neuronal injury in an Aβ25-35-induced Alzheimer's disease rat model via the AKT/GSK-3β pathway

被引:23
作者
Sun, Yueshan [1 ]
Wu, Anguo [1 ,2 ]
Li, Xiu [1 ,3 ]
Qin, Dalian [1 ,2 ]
Jin, Bingjin [4 ,5 ]
Liu, Jian [1 ,2 ]
Tang, Yong [1 ,2 ]
Wu, Jianming [1 ,2 ]
Yu, Chonglin [2 ,6 ]
机构
[1] Southwest Med Univ, Sch Pharm, Dept Pharmacol, 1 Sect 1,Xiang Lin Rd, Luzhou 646000, Peoples R China
[2] Southwest Med Univ, Inst Cardiovasc Res, Key Lab Med Electrophysiol, Luzhou, Peoples R China
[3] Chengdu Med Coll, Dept Anat & Histol & Embryol, Chengdu, Sichuan, Peoples R China
[4] Chengdu Med Collage, Dept Human Anat, Chengdu, Sichuan, Peoples R China
[5] Qinghai Prov Peoples Hosp, Pharm Dept, Xining, Qinghai, Peoples R China
[6] Southwest Med Univ, Sch Preclin Med, Dept Human Anat, Luzhou, Sichuan, Peoples R China
基金
中国国家自然科学基金;
关键词
Litchi chinensis seed fraction; neuroprotection; AD; botanical drug; cognitive function; beta-amyloid; tau; AKT; GSK-3; beta; FOCAL CEREBRAL-ISCHEMIA; AMYLOID-BETA; PI3K/AKT/GSK-3-BETA PATHWAY; TAU HYPERPHOSPHORYLATION; POLYPHENOL EXTRACTS; SIGNALING PATHWAY; OXIDATIVE STRESS; IN-VITRO; APOPTOSIS; PROTEIN;
D O I
10.1080/13880209.2019.1697298
中图分类号
Q94 [植物学];
学科分类号
071001 ;
摘要
Context: The seed of Litchi chinensis Sonn., a famous traditional Chinese medicine, was recently reported to enhance cognitive function by inhibiting neuronal apoptosis in rats. Objective: We determined whether the seed of Litchi chinensis fraction (SLF) can ameliorate hippocampal neuronal injury via the AKT/GSK-3 beta pathway. Materials and methods: We established Alzheimer's disease (AD) model by infusing A beta(25-35) into the lateral ventricle of Sprague-Dawley (SD) rats and randomly divided into five groups (n = 10): sham, donepezil and SLF (120, 240 and 480 mg/kg/d). Rats were treated by intragastric administration for 28 consecutive days. Spatial learning and memory were evaluated with Morris water maze, while protein expression of AKT, GSK-3 beta and tau in the hippocampal neurons was measured by Western blotting and immunohistochemistry. Results: On the fifth day, escape latency of the AD model group was 45.78 +/- 2.52 s and that of the sham operative group was 15.98 +/- 2.32 s. SLF could improve cognitive functions by increasing the number of rats that crossed the platform (p < 0.01), and their platform quadrant dwell time (p < 0.05). The protein expression level of AKT was upregulated (p < 0.001), while that of GSK-3 beta and tau (p < 0.01) was remarkably downregulated in the hippocampal CA1 area. Discussion and conclusions: To our knowledge, the present study is the first to show that SLF may exert neuroprotective effect in AD rats via the AKT/GSK-3 beta signalling pathway, thereby serving as evidence for the potential utility of SLF as an effective drug against AD.
引用
收藏
页码:35 / 43
页数:9
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