Apelin–13 protects against memory impairment and neuronal loss, Induced by Scopolamine in male rats

被引:0
作者
Sara Gazmeh
Maryam Azhir
Leila Elyasi
Mehrdad Jahanshahi
Emsehgol Nikmahzar
Seyed Behnamedin Jameie
机构
[1] Golestan University of Medical Sciences,Neuroscience Research Center
[2] Golestan University of Medical Sciences,Neuroscience Research Center, Department of Anatomy, Faculty of Medicine
[3] Iran University of Medical Sciences,Neuroscience Research Center, Department of Anatomy, Faculty of Medicine
来源
Metabolic Brain Disease | 2022年 / 37卷
关键词
Alzheimer’s disease (AD); Scopolamine; hippocampus; Neuronal density; Avoidance reaction; Apelin–13; Synaptic plasticity;
D O I
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中图分类号
学科分类号
摘要
The present study aimed to evaluate the effects of Apelin–13 on scopolamine–induced memory impairment in rats. Forty male rats were divided into five groups of eight. The control group received no intervention; the scopolamine group underwent stereotaxic surgery and received 3 mg/kg intraperitoneal scopolamine. The treatment groups additionally received 1.25, 2.5 and 5 µg apelin–13 in right lateral ventricles for 7 days. All rats (except the control group) were tested for the passive avoidance reaction, 24 h after the last drug injection. For histological analysis, hippocampal sections were stained with cresyl violet; synaptogenesis biochemical markers were determined by immunoblotting. Apelin–13 alleviated scopolamine–induced passive avoidance memory impairment and neuronal loss in the rats’ hippocampus (P<0.001). The reduction observed in mean concentrations of hippocampal synaptic proteins (including neurexin1, neuroligin, and postsynaptic density protein 95) in scopolamine–treated animals was attenuated by apelin–13 treatment. The results demonstrated that apelin–13 can protect against passive avoidance memory deficiency, and neuronal loss, induced by scopolamine in male rats. Further experimental and clinical studies are required to confirm its therapeutic potential in neurodegenerative diseases.
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页码:701 / 709
页数:8
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