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

• Main Authors: Yueshan Sun, Anguo Wu, Xiu Li, Dalian Qin, Bingjin Jin, Jian Liu, Yong Tang, Jianming Wu, Chonglin Yu
• Format: Article
• Language: English
• Published: Taylor & Francis Group 2020-01-01
• Series: Pharmaceutical Biology
• Subjects: litchi chinensis seed fraction; neuroprotection; ad; botanical drug; cognitive function; beta-amyloid; tau; akt; gsk-3β
• Online Access: http://dx.doi.org/10.1080/13880209.2019.1697298
• ISSN: 1388-0209; 1744-5116

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-3β pathway. Materials and methods We established Alzheimer’s disease (AD) model by infusing Aβ25-35 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-3β 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-3β 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-3β signalling pathway, thereby serving as evidence for the potential utility of SLF as an effective drug against AD.