Synergistic neuroprotection of chitosan-cannabidiol nanoparticles in a rat model of Alzheimer's disease: Amelioration of cognitive deficits and neuroinflammation.

IF 3.1 3区 医学 Q2 NEUROSCIENCES
Zahra Naserramezani, Mohammad Reza Palizvan, Ali Ganji, Ali Ghazavi, Ghasem Mosayebi
{"title":"Synergistic neuroprotection of chitosan-cannabidiol nanoparticles in a rat model of Alzheimer's disease: Amelioration of cognitive deficits and neuroinflammation.","authors":"Zahra Naserramezani, Mohammad Reza Palizvan, Ali Ganji, Ali Ghazavi, Ghasem Mosayebi","doi":"10.1177/13872877251379420","DOIUrl":null,"url":null,"abstract":"<p><p>BackgroundAlzheimer's disease (AD) is a progressive neurodegenerative disorder characterized by cognitive decline, neuroinflammation, and oxidative stress. Current treatments are largely symptomatic, necessitating novel neuroprotective strategies.ObjectiveThis study aimed to investigate the anti-inflammatory and antioxidant effects of chitosan-cannabidiol (CS-CBD) nanoparticles in a streptozotocin (STZ)-induced rat model of AD.MethodsSixty male Wistar rats were randomly divided into five groups: control, AD model (STZ-induced), chitosan-treated, cannabidiol-treated, and CS-CBD-treated. AD was induced by intracerebroventricular injection of STZ (3 mg/kg). Treatments were administered intranasally for 21 days. Cognitive performance was assessed using the Morris water maze. After treatment, oxidative stress markers (NO, FRAP), liver enzymes (ALT, AST), and the expression of inflammatory and neuroprotective genes (IL1β, IL6, IL10, iNOS, PPARγ, BDNF) were evaluated by real-time PCR. Histological analysis of the hippocampus was also performed. Data were analyzed using one-way ANOVA and Tukey's post hoc test (p < 0.05).ResultsThe AD group showed significant impairments in memory and learning (p < 0.0001), increased oxidative stress, and upregulation of pro-inflammatory genes (IL1β, iNOS), with decreased neuroprotective markers (BDNF, PPARγ). CS-CBD treatment significantly improved cognitive function (p < 0.001), restored oxidative balance, reduced IL1β and iNOS expression, and elevated BDNF and PPARγ expression (p < 0.05). Histological analysis confirmed reduced neuronal degeneration and increased neuronal density in the CS-CBD group.ConclusionsCS-CBD nanoparticles exerted potent neuroprotective, antioxidant, and anti-inflammatory effects in an STZ-induced rat model of AD. These findings support the potential of CS-CBD nanoparticles as a promising adjunctive therapy for AD, warranting further investigation.</p>","PeriodicalId":14929,"journal":{"name":"Journal of Alzheimer's Disease","volume":" ","pages":"13872877251379420"},"PeriodicalIF":3.1000,"publicationDate":"2025-09-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Journal of Alzheimer's Disease","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.1177/13872877251379420","RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q2","JCRName":"NEUROSCIENCES","Score":null,"Total":0}
引用次数: 0

Abstract

BackgroundAlzheimer's disease (AD) is a progressive neurodegenerative disorder characterized by cognitive decline, neuroinflammation, and oxidative stress. Current treatments are largely symptomatic, necessitating novel neuroprotective strategies.ObjectiveThis study aimed to investigate the anti-inflammatory and antioxidant effects of chitosan-cannabidiol (CS-CBD) nanoparticles in a streptozotocin (STZ)-induced rat model of AD.MethodsSixty male Wistar rats were randomly divided into five groups: control, AD model (STZ-induced), chitosan-treated, cannabidiol-treated, and CS-CBD-treated. AD was induced by intracerebroventricular injection of STZ (3 mg/kg). Treatments were administered intranasally for 21 days. Cognitive performance was assessed using the Morris water maze. After treatment, oxidative stress markers (NO, FRAP), liver enzymes (ALT, AST), and the expression of inflammatory and neuroprotective genes (IL1β, IL6, IL10, iNOS, PPARγ, BDNF) were evaluated by real-time PCR. Histological analysis of the hippocampus was also performed. Data were analyzed using one-way ANOVA and Tukey's post hoc test (p < 0.05).ResultsThe AD group showed significant impairments in memory and learning (p < 0.0001), increased oxidative stress, and upregulation of pro-inflammatory genes (IL1β, iNOS), with decreased neuroprotective markers (BDNF, PPARγ). CS-CBD treatment significantly improved cognitive function (p < 0.001), restored oxidative balance, reduced IL1β and iNOS expression, and elevated BDNF and PPARγ expression (p < 0.05). Histological analysis confirmed reduced neuronal degeneration and increased neuronal density in the CS-CBD group.ConclusionsCS-CBD nanoparticles exerted potent neuroprotective, antioxidant, and anti-inflammatory effects in an STZ-induced rat model of AD. These findings support the potential of CS-CBD nanoparticles as a promising adjunctive therapy for AD, warranting further investigation.

壳聚糖-大麻二酚纳米颗粒在阿尔茨海默病大鼠模型中的协同神经保护作用:改善认知缺陷和神经炎症。
阿尔茨海默病(AD)是一种以认知能力下降、神经炎症和氧化应激为特征的进行性神经退行性疾病。目前的治疗主要是对症治疗,需要新的神经保护策略。目的研究壳聚糖-大麻二酚(CS-CBD)纳米颗粒对链脲佐菌素(STZ)诱导的AD大鼠模型的抗炎和抗氧化作用。方法雄性Wistar大鼠60只,随机分为5组:对照组、AD模型(stz诱导)组、壳聚糖组、大麻二酚组和cs - cbd组。脑室内注射STZ (3 mg/kg)诱导AD。经鼻给药21天。使用Morris水迷宫评估认知表现。治疗后,采用实时荧光定量PCR检测氧化应激标志物(NO、FRAP)、肝酶(ALT、AST)以及炎症和神经保护基因(IL1β、IL6、IL10、iNOS、PPARγ、BDNF)的表达。同时对海马进行组织学分析。数据分析采用单因素方差分析和Tukey事后检验(p
本文章由计算机程序翻译,如有差异,请以英文原文为准。
求助全文
约1分钟内获得全文 求助全文
来源期刊
Journal of Alzheimer's Disease
Journal of Alzheimer's Disease 医学-神经科学
CiteScore
6.40
自引率
7.50%
发文量
1327
审稿时长
2 months
期刊介绍: The Journal of Alzheimer''s Disease (JAD) is an international multidisciplinary journal to facilitate progress in understanding the etiology, pathogenesis, epidemiology, genetics, behavior, treatment and psychology of Alzheimer''s disease. The journal publishes research reports, reviews, short communications, hypotheses, ethics reviews, book reviews, and letters-to-the-editor. The journal is dedicated to providing an open forum for original research that will expedite our fundamental understanding of Alzheimer''s disease.
×
引用
GB/T 7714-2015
复制
MLA
复制
APA
复制
导出至
BibTeX EndNote RefMan NoteFirst NoteExpress
×
提示
您的信息不完整,为了账户安全,请先补充。
现在去补充
×
提示
您因"违规操作"
具体请查看互助需知
我知道了
×
提示
确定
请完成安全验证×
copy
已复制链接
快去分享给好友吧!
我知道了
右上角分享
点击右上角分享
0
联系我们:info@booksci.cn Book学术提供免费学术资源搜索服务,方便国内外学者检索中英文文献。致力于提供最便捷和优质的服务体验。 Copyright © 2023 布克学术 All rights reserved.
京ICP备2023020795号-1
ghs 京公网安备 11010802042870号
Book学术文献互助
Book学术文献互助群
群 号:604180095
Book学术官方微信