Rania Magadmi, Sara Nassibi, Fatemah Kamel, Aziza R Al-Rafiah, Duaa Bakhshwin, Maha Jamal, Mohammed Alsieni, Abdulhadi S Burzangi, M A F Zaher, Mohammed Bendary
{"title":"虾青素对东莨菪碱诱导的阿尔茨海默氏症小鼠模型的保护作用。","authors":"Rania Magadmi, Sara Nassibi, Fatemah Kamel, Aziza R Al-Rafiah, Duaa Bakhshwin, Maha Jamal, Mohammed Alsieni, Abdulhadi S Burzangi, M A F Zaher, Mohammed Bendary","doi":"10.17712/nsj.2024.2.20230060","DOIUrl":null,"url":null,"abstract":"<p><strong>Objectives: </strong>To investigate the fundamental mechanisms of the neuroprotective impact of Astaxanthin (AST) in a mouse model of Alzheimer's disease (AD) induced by scopolamine.</p><p><strong>Methods: </strong>This research constituted an in vivo animal study encompassing 36 adult male mice, divided into 6 groups: Control, 100 mg/kg AST, 2 mg/kg scopolamine (AD group), 100 mg/kg AST+2 mg/kg scopolamine, 3 mg/kg galantamine+2 mg/kg scopolamine, and 100 mg/kg AST+3 mg/kg galantamine+2 mg/kg scopolamine. After 14 days, the mice's short-term memory, hippocampus tissue, oxidative and inflammatory markers were evaluated.</p><p><strong>Results: </strong>The AST demonstrated a beneficial influence on short-term memory and a reduction in acetylcholinesterase activity in the brain. It exhibited neuroprotective and anti-amyloidogenic properties, significantly decreased pro-inflammatory markers and oxidative stress, and reversed the decline of the Akt-1 and phosphorylated Akt pathway, a crucial regulator of abnormal tau. Furthermore, AST enhanced the effect of galantamine in reducing inflammation and oxidative stress.</p><p><strong>Conclusion: </strong>The findings indicate that AST may offer therapeutic benefits against cognitive dysfunction in AD. This is attributed to its ability to reduce oxidative stress, control neuroinflammation, and enhance Akt-1 and pAkt levels, thereby underscoring its potential in AD treatment strategies.</p>","PeriodicalId":19284,"journal":{"name":"Neurosciences","volume":null,"pages":null},"PeriodicalIF":1.2000,"publicationDate":"2024-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11305357/pdf/","citationCount":"0","resultStr":"{\"title\":\"The protective effect of Astaxanthin on scopolamine - induced Alzheimer's model in mice.\",\"authors\":\"Rania Magadmi, Sara Nassibi, Fatemah Kamel, Aziza R Al-Rafiah, Duaa Bakhshwin, Maha Jamal, Mohammed Alsieni, Abdulhadi S Burzangi, M A F Zaher, Mohammed Bendary\",\"doi\":\"10.17712/nsj.2024.2.20230060\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><strong>Objectives: </strong>To investigate the fundamental mechanisms of the neuroprotective impact of Astaxanthin (AST) in a mouse model of Alzheimer's disease (AD) induced by scopolamine.</p><p><strong>Methods: </strong>This research constituted an in vivo animal study encompassing 36 adult male mice, divided into 6 groups: Control, 100 mg/kg AST, 2 mg/kg scopolamine (AD group), 100 mg/kg AST+2 mg/kg scopolamine, 3 mg/kg galantamine+2 mg/kg scopolamine, and 100 mg/kg AST+3 mg/kg galantamine+2 mg/kg scopolamine. After 14 days, the mice's short-term memory, hippocampus tissue, oxidative and inflammatory markers were evaluated.</p><p><strong>Results: </strong>The AST demonstrated a beneficial influence on short-term memory and a reduction in acetylcholinesterase activity in the brain. It exhibited neuroprotective and anti-amyloidogenic properties, significantly decreased pro-inflammatory markers and oxidative stress, and reversed the decline of the Akt-1 and phosphorylated Akt pathway, a crucial regulator of abnormal tau. Furthermore, AST enhanced the effect of galantamine in reducing inflammation and oxidative stress.</p><p><strong>Conclusion: </strong>The findings indicate that AST may offer therapeutic benefits against cognitive dysfunction in AD. This is attributed to its ability to reduce oxidative stress, control neuroinflammation, and enhance Akt-1 and pAkt levels, thereby underscoring its potential in AD treatment strategies.</p>\",\"PeriodicalId\":19284,\"journal\":{\"name\":\"Neurosciences\",\"volume\":null,\"pages\":null},\"PeriodicalIF\":1.2000,\"publicationDate\":\"2024-05-01\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11305357/pdf/\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Neurosciences\",\"FirstCategoryId\":\"3\",\"ListUrlMain\":\"https://doi.org/10.17712/nsj.2024.2.20230060\",\"RegionNum\":4,\"RegionCategory\":\"医学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q4\",\"JCRName\":\"CLINICAL NEUROLOGY\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Neurosciences","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.17712/nsj.2024.2.20230060","RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q4","JCRName":"CLINICAL NEUROLOGY","Score":null,"Total":0}
引用次数: 0
摘要
目的研究虾青素(AST)对东莨菪碱诱导的阿尔茨海默病(AD)小鼠模型神经保护作用的基本机制:本研究是一项体内动物研究,包括36只成年雄性小鼠,分为6组:对照组、100毫克/千克AST组、2毫克/千克东莨菪碱组(AD组)、100毫克/千克AST+2毫克/千克东莨菪碱组、3毫克/千克加兰他敏+2毫克/千克东莨菪碱组和100毫克/千克AST+3毫克/千克加兰他敏+2毫克/千克东莨菪碱组。14 天后,对小鼠的短期记忆、海马组织、氧化和炎症指标进行了评估:结果:AST 对小鼠的短期记忆产生了有益的影响,并降低了大脑中乙酰胆碱酯酶的活性。它还具有神经保护和抗淀粉样蛋白生成的特性,显著降低了促炎症标志物和氧化应激,并逆转了 Akt-1 和磷酸化 Akt 通路(异常 tau 的关键调节因子)的衰退。此外,AST还能增强加兰他敏在减少炎症和氧化应激方面的作用:结论:研究结果表明,AST 可为治疗认知功能障碍提供益处。结论:研究结果表明,AST可能对AD患者的认知功能障碍有治疗作用,这归因于它能够减少氧化应激、控制神经炎症、提高Akt-1和pAkt水平,从而突出了它在AD治疗策略中的潜力。
The protective effect of Astaxanthin on scopolamine - induced Alzheimer's model in mice.
Objectives: To investigate the fundamental mechanisms of the neuroprotective impact of Astaxanthin (AST) in a mouse model of Alzheimer's disease (AD) induced by scopolamine.
Methods: This research constituted an in vivo animal study encompassing 36 adult male mice, divided into 6 groups: Control, 100 mg/kg AST, 2 mg/kg scopolamine (AD group), 100 mg/kg AST+2 mg/kg scopolamine, 3 mg/kg galantamine+2 mg/kg scopolamine, and 100 mg/kg AST+3 mg/kg galantamine+2 mg/kg scopolamine. After 14 days, the mice's short-term memory, hippocampus tissue, oxidative and inflammatory markers were evaluated.
Results: The AST demonstrated a beneficial influence on short-term memory and a reduction in acetylcholinesterase activity in the brain. It exhibited neuroprotective and anti-amyloidogenic properties, significantly decreased pro-inflammatory markers and oxidative stress, and reversed the decline of the Akt-1 and phosphorylated Akt pathway, a crucial regulator of abnormal tau. Furthermore, AST enhanced the effect of galantamine in reducing inflammation and oxidative stress.
Conclusion: The findings indicate that AST may offer therapeutic benefits against cognitive dysfunction in AD. This is attributed to its ability to reduce oxidative stress, control neuroinflammation, and enhance Akt-1 and pAkt levels, thereby underscoring its potential in AD treatment strategies.
期刊介绍:
Neurosciences is an open access, peer-reviewed, quarterly publication. Authors are invited to submit for publication articles reporting original work related to the nervous system, e.g., neurology, neurophysiology, neuroradiology, neurosurgery, neurorehabilitation, neurooncology, neuropsychiatry, and neurogenetics, etc. Basic research withclear clinical implications will also be considered. Review articles of current interest and high standard are welcomed for consideration. Prospective workshould not be backdated. There are also sections for Case Reports, Brief Communication, Correspondence, and medical news items. To promote continuous education, training, and learning, we include Clinical Images and MCQ’s. Highlights of international and regional meetings of interest, and specialized supplements will also be considered. All submissions must conform to the Uniform Requirements.