Agmatine prevents the memory impairment and the dysfunction of hippocampal GSK-3β and ERK signaling induced by aluminum nanoparticle in mice.

IF 1.6 4区 心理学 Q3 BEHAVIORAL SCIENCES
Sadegh Izadi, Amin Rezaei, Zahra Esmaili, Roksana Soukhaklari, Maryam Moosavi
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引用次数: 1

Abstract

The growing usage of aluminum nanoparticles (Al-NP) and their exposure may influence body function. Considering the proposed relationship between Al and the pathogenesis of Alzheimer's disease and the concern about the effect of this nanoparticle on brain health and cognitive function, the use of neuroprotective agents might be helpful. According to the reported neuroprotective effects of agmatine, in the present study, the possible protective effect of agmatine was assessed in mice model of Al-NP-induced memory impairment. In addition, due to the roles of hippocampal Glycogen synthase kinase-3 beta (GSK-3β) and ERK signaling in memory and its disorders, these pathways were also investigated. Al-NP (10 mg/kg/p.o.) with/without agmatine (5 or 10 mg/kg/i.p.) was administered to adult male NMRI mice for 5 days. Novel object recognition (NOR) test session was used to assess cognitive function. Following the behavioral assessments, the hippocampi were used to determine the phosphorylated and total levels of GSK-3β and ERK as well as GAPDH using western blot analysis. The results showed that Al-NP impaired NOR memory in mice while agmatine 10 mg/kg prevented the memory deficit induced by Al-NP. Furthermore, Al-NP activated GSK-3β as well as ERK signals within the hippocampus while agmatine prevented the effects of Al-NP on GSK-3β and ERK signals within the hippocampus. Besides supporting the neuroprotective effects of agmatine, these findings suggest the possibility of the connection of hippocampal GSK-3β and ERK signaling in the neuroprotective effect of this polyamine against Al-NP.

胍丁氨酸对铝纳米颗粒诱导的小鼠记忆损伤及海马GSK-3β和ERK信号传导功能障碍具有预防作用。
纳米铝颗粒(Al-NP)的日益广泛使用及其暴露可能会影响人体功能。考虑到人工智能与阿尔茨海默病发病机制之间的关系,以及这种纳米颗粒对大脑健康和认知功能的影响,使用神经保护剂可能会有所帮助。根据已报道的agmatine的神经保护作用,本研究在al - np诱导的小鼠记忆损伤模型中评估了agmatine可能的保护作用。此外,由于海马糖原合成酶激酶-3β (GSK-3β)和ERK信号在记忆及其障碍中的作用,这些途径也被研究。Al-NP (10 mg/kg/p.o)加/不加胍丁氨酸(5或10 mg/kg/i.p)给成年雄性NMRI小鼠5天。新目标识别(NOR)测试用于评估认知功能。行为评估后,采用western blot方法测定海马GSK-3β、ERK和GAPDH的磷酸化水平和总水平。结果表明,Al-NP可使小鼠NOR记忆受损,而10 mg/kg的胍丁氨酸可防止Al-NP引起的记忆缺损。此外,Al-NP激活海马内GSK-3β和ERK信号,而胍丁氨酸阻止Al-NP对海马内GSK-3β和ERK信号的影响。除了支持agmatine的神经保护作用外,这些发现表明海马GSK-3β和ERK信号通路可能在这种多胺对Al-NP的神经保护作用中起作用。
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来源期刊
Behavioural Pharmacology
Behavioural Pharmacology 医学-行为科学
CiteScore
3.40
自引率
0.00%
发文量
84
审稿时长
6-12 weeks
期刊介绍: Behavioural Pharmacology accepts original full and short research reports in diverse areas ranging from ethopharmacology to the pharmacology of schedule-controlled operant behaviour, provided that their primary focus is behavioural. Suitable topics include drug, chemical and hormonal effects on behaviour, the neurochemical mechanisms under-lying behaviour, and behavioural methods for the study of drug action. Both animal and human studies are welcome; however, studies reporting neurochemical data should have a predominantly behavioural focus, and human studies should not consist exclusively of clinical trials or case reports. Preference is given to studies that demonstrate and develop the potential of behavioural methods, and to papers reporting findings of direct relevance to clinical problems. Papers making a significant theoretical contribution are particularly welcome and, where possible and merited, space is made available for authors to explore fully the theoretical implications of their findings. Reviews of an area of the literature or at an appropriate stage in the development of an author’s own work are welcome. Commentaries in areas of current interest are also considered for publication, as are Reviews and Commentaries in areas outside behavioural pharmacology, but of importance and interest to behavioural pharmacologists. Behavioural Pharmacology publishes frequent Special Issues on current hot topics. The editors welcome correspondence about whether a paper in preparation might be suitable for inclusion in a Special Issue.
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