β-sitosterol Protects against Aluminium Chloride-mediated Neurotoxicity.

IF 1.8 4区医学 Q3 CLINICAL NEUROLOGY

Current Alzheimer research Pub Date : 2023-01-01 DOI:10.2174/1567205020666230308151443

Sanjay Yadav, Punita Aggarwal, Faiz Khan, Gopal Khodve, Dibyasundar Padhy, Poonam Yadav, Sugato Banerjee

{"title":"β-sitosterol Protects against Aluminium Chloride-mediated Neurotoxicity.","authors":"Sanjay Yadav, Punita Aggarwal, Faiz Khan, Gopal Khodve, Dibyasundar Padhy, Poonam Yadav, Sugato Banerjee","doi":"10.2174/1567205020666230308151443","DOIUrl":null,"url":null,"abstract":"Objective: The objective of this study is to investigate the neuroprotective effects of β- sitosterol using the AlCl3 model of Alzheimer's Disease.Methods: AlCl3 model was used to study cognition decline and behavioral impairments in C57BL/6 mice. Animals were randomly assigned into 4 groups with the following treatments: Group 1 received normal saline for 21 days, Group 2 received AlCl3 (10 mg/kg) for 14 days; Group 3 received AlCl3(10 mg/kg) for 14 days + β-sitosterol (25mg/kg) for 21 days; while Group 4 was administered β-sitosterol (25mg/kg) for 21 days. On day 22, we performed the behavioral studies using a Y maze, passive avoidance test, and novel object recognition test for all groups. Then the mice were sacrificed. The corticohippocampal region of the brain was isolated for acetylcholinesterase (AChE), acetylcholine (ACh), and GSH estimation. We conducted histopathological studies using Congo red staining to measure β -amyloid deposition in the cortex and hippocampal region for all animal groups.Results: AlCl3 successfully induced cognitive decline in mice following a 14-day induction period, as shown by significantly decreased (p < 0.001) in step-through latency, % alterations, and preference index values. These animals also exhibited a substantial decrease in ACh (p <0.001) and GSH (p < 0.001) and a rise in AChE (p < 0.001) compared to the control group. Mice administered with AlCl3 and β-sitosterol showed significantly higher step-through latency time, % alteration time, and % preference index (p < 0.001) and higher levels of ACh, GSH, and lower levels of AChE in comparison to the AlCl3 model. AlCl3-administered animals also showed higher β-amyloid deposition, which got significantly reduced in the β-sitosterol treated group.Conclusion: AlCl3 was effectively employed to induce a cognitive deficit in mice, resulting in neurochemical changes and cognitive decline. β -sitosterol treatment mitigated AlCl3-mediated cognitive impairment.","PeriodicalId":10810,"journal":{"name":"Current Alzheimer research","volume":null,"pages":null},"PeriodicalIF":1.8000,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Current Alzheimer research","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.2174/1567205020666230308151443","RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q3","JCRName":"CLINICAL NEUROLOGY","Score":null,"Total":0}

引用次数: 0

Abstract

Objective: The objective of this study is to investigate the neuroprotective effects of β- sitosterol using the AlCl3 model of Alzheimer's Disease.

Methods: AlCl₃ model was used to study cognition decline and behavioral impairments in C57BL/6 mice. Animals were randomly assigned into 4 groups with the following treatments: Group 1 received normal saline for 21 days, Group 2 received AlCl₃ (10 mg/kg) for 14 days; Group 3 received AlCl3(10 mg/kg) for 14 days + β-sitosterol (25mg/kg) for 21 days; while Group 4 was administered β-sitosterol (25mg/kg) for 21 days. On day 22, we performed the behavioral studies using a Y maze, passive avoidance test, and novel object recognition test for all groups. Then the mice were sacrificed. The corticohippocampal region of the brain was isolated for acetylcholinesterase (AChE), acetylcholine (ACh), and GSH estimation. We conducted histopathological studies using Congo red staining to measure β -amyloid deposition in the cortex and hippocampal region for all animal groups.

Results: AlCl₃ successfully induced cognitive decline in mice following a 14-day induction period, as shown by significantly decreased (p < 0.001) in step-through latency, % alterations, and preference index values. These animals also exhibited a substantial decrease in ACh (p <0.001) and GSH (p < 0.001) and a rise in AChE (p < 0.001) compared to the control group. Mice administered with AlCl₃ and β-sitosterol showed significantly higher step-through latency time, % alteration time, and % preference index (p < 0.001) and higher levels of ACh, GSH, and lower levels of AChE in comparison to the AlCl₃ model. AlCl3-administered animals also showed higher β-amyloid deposition, which got significantly reduced in the β-sitosterol treated group.

Conclusion: AlCl3 was effectively employed to induce a cognitive deficit in mice, resulting in neurochemical changes and cognitive decline. β -sitosterol treatment mitigated AlCl₃-mediated cognitive impairment.

查看原文本刊更多论文

β-谷甾醇对氯化铝介导的神经毒性具有保护作用。

目的：应用AlCl3阿尔茨海默病模型研究β-谷甾醇的神经保护作用。动物被随机分为4组，治疗如下：第一组接受生理盐水21天，第二组接受AlCl3（10mg/kg）14天；第3组接受AlCl3（10mg/kg）治疗14天+β-谷甾醇（25mg/kg）治疗21天；β-谷甾醇（25mg/kg）给药21天。第22天，我们使用Y迷宫、被动回避测试和新型物体识别测试对所有组进行了行为研究。然后处死小鼠。分离大脑的皮质海马区进行乙酰胆碱酯酶（AChE）、乙酰胆碱（ACh）和谷胱甘肽的估计。我们使用刚果红染色进行了组织病理学研究，以测量所有动物组大脑皮层和海马区的β-淀粉样蛋白沉积。结果：AlCl3在14天的诱导期后成功诱导小鼠认知能力下降，表现为通过潜伏期、%变化和偏好指数值的步进显著降低（p＜0.001）。与AlCl3模型相比，这些动物的ACh（p3和β-谷甾醇表现出显著更高的潜伏期、%改变时间和%偏好指数（p＜0.001），ACh、GSH水平更高，AChE水平更低。AlCl3给药的动物也表现出更高的β-淀粉样蛋白沉积，在β-谷甾醇治疗组中显著减少。结论：AlCl3可有效诱导小鼠认知功能障碍，导致神经化学变化和认知能力下降。β-谷甾醇治疗减轻了AlCl3介导的认知障碍。

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

Current Alzheimer research 医学-神经科学

CiteScore

4.00

自引率

4.80%

发文量

审稿时长

4-8 weeks

期刊介绍： Current Alzheimer Research publishes peer-reviewed frontier review, research, drug clinical trial studies and letter articles on all areas of Alzheimer’s disease. This multidisciplinary journal will help in understanding the neurobiology, genetics, pathogenesis, and treatment strategies of Alzheimer’s disease. The journal publishes objective reviews written by experts and leaders actively engaged in research using cellular, molecular, and animal models. The journal also covers original articles on recent research in fast emerging areas of molecular diagnostics, brain imaging, drug development and discovery, and clinical aspects of Alzheimer’s disease. Manuscripts are encouraged that relate to the synergistic mechanism of Alzheimer''s disease with other dementia and neurodegenerative disorders. Book reviews, meeting reports and letters-to-the-editor are also published. The journal is essential reading for researchers, educators and physicians with interest in age-related dementia and Alzheimer’s disease. Current Alzheimer Research provides a comprehensive ''bird''s-eye view'' of the current state of Alzheimer''s research for neuroscientists, clinicians, health science planners, granting, caregivers and families of this devastating disease.