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Pharm Biol. 2020 Dec;58(1):35-43. doi: 10.1080/13880209.2019.1697298.

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.

Sun Y1, Wu A1,2, Li X1,3, Qin D1,2, Jin B4, Liu J1,2, Tang Y1,2, Wu J1,2, Yu C2.

Author information

1
Department of Pharmacology, School of Pharmacy, Southwest Medical University, Luzhou, China.
2
Institute of Cardiovascular Research, The Key Laboratory of Medical Electrophysiology, Southwest Medical University, Luzhou, China.
3
Department of Anatomy and Histology and Embryology, Chengdu Medical College, Chengdu, China.
4
Department of Human Anatomy, Chengdu Medical Collage, Chengdu, China.

Abstract

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.

KEYWORDS:

AD; AKT; GSK-3β; Litchi chinensis seed fraction; beta-amyloid; botanical drug; cognitive function; neuroprotection; tau

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