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The seed of Litchi chinensis fraction ameliorates hippocampal neuronal injury in an Aβ(25-35)-induced Alzheimer’s disease rat model via the AKT/GSK-3β pathway

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 vi...

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Detalles Bibliográficos
Autores principales: Sun, Yueshan, Wu, Anguo, Li, Xiu, Qin, Dalian, Jin, Bingjin, Liu, Jian, Tang, Yong, Wu, Jianming, Yu, Chonglin
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Taylor & Francis 2019
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6968628/
https://www.ncbi.nlm.nih.gov/pubmed/31881157
http://dx.doi.org/10.1080/13880209.2019.1697298
Descripción
Sumario: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 Aβ(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-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.