{"title":"氧化钇纳米颗粒可减轻链脲佐菌素诱导的认知缺陷、神经炎症和线粒体生物生成损伤。","authors":"","doi":"10.1016/j.neulet.2024.137895","DOIUrl":null,"url":null,"abstract":"<div><p>Alzheimer’s disease (AD) is a common neurodegenerative disorder characterized by progressive cognitive decline. Yttrium oxide nanoparticles (Y<sub>2</sub>O<sub>3</sub>NPs) have recently attracted much attention for their potential anti-inflammatory and antioxidant properties. However, the effects of Y<sub>2</sub>O<sub>3</sub>NPs in animal models of AD are less studied. This study aimed to investigate the potential therapeutic effects of Y<sub>2</sub>O<sub>3</sub>NPs in streptozotocin (STZ)-treated rats, a reliable animal model of AD, with special emphasis on cognitive function, neuroinflammation, and mitochondrial biogenesis in the hippocampus. Male Wistar rats were stereotaxically injected with STZ (3 mg/kg, 3 µl/ventricle). Three weeks after STZ injection, cognitive function was assessed using the Morris water maze, elevated plus maze, and passive avoidance tasks. Intraperitoneal treatment with Y<sub>2</sub>O<sub>3</sub>NPs (0.1, 0.3, or 0.5 mg/kg) was started 24 h after the STZ injection and continued for 21 days. The mRNA and protein levels of pro-inflammatory cytokines (TNF-α, IL-6, and IL-1β) and components involved in mitochondrial biogenesis (PGC-1α, NRF-1, and TFAM) were measured in the hippocampus. The results indicated that STZ induced cognitive impairment and led to neuroinflammation and mitochondrial biogenesis impairment in the hippocampus of rats. Interestingly, treatment with Y<sub>2</sub>O<sub>3</sub>NPs effectively reduced STZ-induced cognitive deficits in a dose-dependent manner, possibly by attenuating neuroinflammation and mitochondrial biogenesis impairment. These findings suggest that Y<sub>2</sub>O<sub>3</sub>NPs can be considered as a promising therapeutic agent for treating or ameliorating the neuropathological effects associated with AD.</p></div>","PeriodicalId":19290,"journal":{"name":"Neuroscience Letters","volume":null,"pages":null},"PeriodicalIF":2.5000,"publicationDate":"2024-07-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"Yttrium oxide nanoparticles alleviate cognitive deficits, neuroinflammation, and mitochondrial biogenesis impairment induced by streptozotocin\",\"authors\":\"\",\"doi\":\"10.1016/j.neulet.2024.137895\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<div><p>Alzheimer’s disease (AD) is a common neurodegenerative disorder characterized by progressive cognitive decline. Yttrium oxide nanoparticles (Y<sub>2</sub>O<sub>3</sub>NPs) have recently attracted much attention for their potential anti-inflammatory and antioxidant properties. However, the effects of Y<sub>2</sub>O<sub>3</sub>NPs in animal models of AD are less studied. This study aimed to investigate the potential therapeutic effects of Y<sub>2</sub>O<sub>3</sub>NPs in streptozotocin (STZ)-treated rats, a reliable animal model of AD, with special emphasis on cognitive function, neuroinflammation, and mitochondrial biogenesis in the hippocampus. Male Wistar rats were stereotaxically injected with STZ (3 mg/kg, 3 µl/ventricle). Three weeks after STZ injection, cognitive function was assessed using the Morris water maze, elevated plus maze, and passive avoidance tasks. Intraperitoneal treatment with Y<sub>2</sub>O<sub>3</sub>NPs (0.1, 0.3, or 0.5 mg/kg) was started 24 h after the STZ injection and continued for 21 days. The mRNA and protein levels of pro-inflammatory cytokines (TNF-α, IL-6, and IL-1β) and components involved in mitochondrial biogenesis (PGC-1α, NRF-1, and TFAM) were measured in the hippocampus. The results indicated that STZ induced cognitive impairment and led to neuroinflammation and mitochondrial biogenesis impairment in the hippocampus of rats. Interestingly, treatment with Y<sub>2</sub>O<sub>3</sub>NPs effectively reduced STZ-induced cognitive deficits in a dose-dependent manner, possibly by attenuating neuroinflammation and mitochondrial biogenesis impairment. These findings suggest that Y<sub>2</sub>O<sub>3</sub>NPs can be considered as a promising therapeutic agent for treating or ameliorating the neuropathological effects associated with AD.</p></div>\",\"PeriodicalId\":19290,\"journal\":{\"name\":\"Neuroscience Letters\",\"volume\":null,\"pages\":null},\"PeriodicalIF\":2.5000,\"publicationDate\":\"2024-07-19\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Neuroscience Letters\",\"FirstCategoryId\":\"3\",\"ListUrlMain\":\"https://www.sciencedirect.com/science/article/pii/S0304394024002738\",\"RegionNum\":4,\"RegionCategory\":\"医学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q3\",\"JCRName\":\"NEUROSCIENCES\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Neuroscience Letters","FirstCategoryId":"3","ListUrlMain":"https://www.sciencedirect.com/science/article/pii/S0304394024002738","RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q3","JCRName":"NEUROSCIENCES","Score":null,"Total":0}
Yttrium oxide nanoparticles alleviate cognitive deficits, neuroinflammation, and mitochondrial biogenesis impairment induced by streptozotocin
Alzheimer’s disease (AD) is a common neurodegenerative disorder characterized by progressive cognitive decline. Yttrium oxide nanoparticles (Y2O3NPs) have recently attracted much attention for their potential anti-inflammatory and antioxidant properties. However, the effects of Y2O3NPs in animal models of AD are less studied. This study aimed to investigate the potential therapeutic effects of Y2O3NPs in streptozotocin (STZ)-treated rats, a reliable animal model of AD, with special emphasis on cognitive function, neuroinflammation, and mitochondrial biogenesis in the hippocampus. Male Wistar rats were stereotaxically injected with STZ (3 mg/kg, 3 µl/ventricle). Three weeks after STZ injection, cognitive function was assessed using the Morris water maze, elevated plus maze, and passive avoidance tasks. Intraperitoneal treatment with Y2O3NPs (0.1, 0.3, or 0.5 mg/kg) was started 24 h after the STZ injection and continued for 21 days. The mRNA and protein levels of pro-inflammatory cytokines (TNF-α, IL-6, and IL-1β) and components involved in mitochondrial biogenesis (PGC-1α, NRF-1, and TFAM) were measured in the hippocampus. The results indicated that STZ induced cognitive impairment and led to neuroinflammation and mitochondrial biogenesis impairment in the hippocampus of rats. Interestingly, treatment with Y2O3NPs effectively reduced STZ-induced cognitive deficits in a dose-dependent manner, possibly by attenuating neuroinflammation and mitochondrial biogenesis impairment. These findings suggest that Y2O3NPs can be considered as a promising therapeutic agent for treating or ameliorating the neuropathological effects associated with AD.
期刊介绍:
Neuroscience Letters is devoted to the rapid publication of short, high-quality papers of interest to the broad community of neuroscientists. Only papers which will make a significant addition to the literature in the field will be published. Papers in all areas of neuroscience - molecular, cellular, developmental, systems, behavioral and cognitive, as well as computational - will be considered for publication. Submission of laboratory investigations that shed light on disease mechanisms is encouraged. Special Issues, edited by Guest Editors to cover new and rapidly-moving areas, will include invited mini-reviews. Occasional mini-reviews in especially timely areas will be considered for publication, without invitation, outside of Special Issues; these un-solicited mini-reviews can be submitted without invitation but must be of very high quality. Clinical studies will also be published if they provide new information about organization or actions of the nervous system, or provide new insights into the neurobiology of disease. NSL does not publish case reports.