The Effect of Cannabidiol Coated by Nano-Chitosan on Learning and Memory, Hippocampal CB1 and CB2 Levels, and Amyloid Plaques in an Alzheimer's Disease Rat Model.

IF 2.3 4区 心理学 Q3 NEUROSCIENCES
Neuropsychobiology Pub Date : 2022-01-01 Epub Date: 2021-11-02 DOI:10.1159/000519534
Mohammadali Amini, Zohreh Abdolmaleki
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引用次数: 11

Abstract

Introduction: Using nanoparticle (NP) drugs can have better effects on the target tissue in various diseases. Alzheimer's disease (AD) is one of the degenerative neurological diseases that due to its high prevalence, requires the use of more appropriate treatments. Therefore, the aim of this study was consideration of the effect of cannabidiol (CBD) coated by nano-chitosan on learning and memory, hippocampal cannabinoid receptor type 1 (CB1) and cannabinoid receptor type 1 (CB2) levels, and amyloid plaques in an AD rat model.

Material and methods: Thirty-five male Wistar rats were randomly divided into 5 groups (n = 7 in each): control, Alzheimer's disease model that received the beta-amyloid (Aβ) peptide (Alz), Alz + nano-chitosan (NP) Alz + CBD, and Alz + NP + CBD. Alz was induced by injection of the Aβ1-42 peptide into the hippocampal area cornu ammonis1. After confirmation of Alz, 1 μL of CBD and NP + CBD were administered by oral gavage daily in rats for 1 month. The Morris water maze (MWM) test was used to assess learning and memory of animals. Cresyl violet staining was used for consideration of dead cells. Gene and protein expression of CB1 and CB2 was performed by real-time PCR and immunohistochemistry methods.

Results: Induction of Alz significantly increased Aβ plaques and dead cells compared to the control group (p < 0.001). Results of MWM in the day test show that Alz + NP + CBD significantly decrease escape latency (p < 0.01), travelled distance (p < 0.001), and significantly increased spending time (p < 0.001) compared to the Alz group. Protein expression of CB1 and CB2 significantly increased in Alz + CBD and Alz + NP + CBD compared to the Alz group (p < 0.05).

Conclusion: It seems that CBD coated by nano-chitosan has good potential for reducing Aβ plaques, increasing brain CB1 and levels CB2, and improving learning and memory in Alz rats.

纳米壳聚糖包被大麻二酚对阿尔茨海默病模型大鼠学习记忆、海马CB1和CB2水平及淀粉样斑块的影响
在多种疾病中,使用纳米颗粒(NP)药物对靶组织有更好的作用。阿尔茨海默病(AD)是一种退行性神经系统疾病,由于其高患病率,需要使用更合适的治疗方法。因此,本研究旨在探讨纳米壳聚糖包被的大麻二酚(CBD)对AD大鼠学习记忆、海马大麻素受体1型(CB1)和大麻素受体1型(CB2)水平和淀粉样斑块的影响。材料与方法:35只雄性Wistar大鼠随机分为5组(每组7只):对照组、阿尔茨海默病模型组,分别给予β -淀粉样蛋白(Aβ)肽(Alz)、Alz +纳米壳聚糖(NP) Alz + CBD、Alz + NP + CBD。通过氨化1向海马区注射Aβ1-42肽诱导Alz。经Alz确认后,大鼠每日灌胃1 μL CBD和NP + CBD,连续灌胃1个月。采用Morris水迷宫(Morris water maze, MWM)试验评价动物的学习记忆能力。采用甲酚紫染色,考虑细胞死亡。采用实时荧光定量PCR和免疫组织化学方法检测CB1和CB2基因和蛋白的表达。结果:与对照组相比,Alz诱导显著增加了Aβ斑块和死细胞(p < 0.001)。白天试验MWM结果显示,与Alz组相比,Alz + NP + CBD显著减少逃避潜伏期(p < 0.01)、行走距离(p < 0.001)和停留时间(p < 0.001)。与Alz组相比,Alz + CBD和Alz + NP + CBD组CB1和CB2蛋白表达显著升高(p < 0.05)。结论:纳米壳聚糖包被的CBD具有减少Alz大鼠Aβ斑块,提高脑CB1和CB2水平,改善学习记忆的良好潜力。
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来源期刊
Neuropsychobiology
Neuropsychobiology 医学-精神病学
CiteScore
7.20
自引率
0.00%
发文量
26
审稿时长
6 months
期刊介绍: The biological approach to mental disorders continues to yield innovative findings of clinical importance, particularly if methodologies are combined. This journal collects high quality empirical studies from various experimental and clinical approaches in the fields of Biological Psychiatry, Biological Psychology and Neuropsychology. It features original, clinical and basic research in the fields of neurophysiology and functional imaging, neuropharmacology and neurochemistry, neuroendocrinology and neuroimmunology, genetics and their relationships with normal psychology and psychopathology. In addition, the reader will find studies on animal models of mental disorders and therapeutic interventions, and pharmacoelectroencephalographic studies. Regular reviews report new methodologic approaches, and selected case reports provide hints for future research. ''Neuropsychobiology'' is a complete record of strategies and methodologies employed to study the biological basis of mental functions including their interactions with psychological and social factors.
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