A New Dipeptide H-MGL Partially Ameliorating Memory Impairment in an STZ-induced Alzheimer Model in Male Rats

一种新型二肽H-MGL可部分改善STZ诱导的雄性大鼠阿尔茨海默病模型中的记忆障碍

阅读:2

Abstract

INTRODUCTION: Alzheimer disease (AD) is a progressive neurodegenerative disorder that is identified by the gradual decline in memory and cognitive function. It is classified by the deposition of Aβ plaques, the build-up of intracellular neurofibrillary tangle (NFT), and neuron loss. Neurotrophic factors play a critical role in the treatment of AD. However, utilizing such neurotrophins has encountered certain difficulties and side effects. Novel technological advancements prioritize innovative dipeptide usage, which offers fewer side effects. METHODS: The present study endeavors to analyze the compound hexamethylenediamide bis-(N-monosuccinyl-glutamyl-lysine) (lab name: H-MGL), a newly discovered neurotrophin mimetic dipeptide, to alleviate memory impairment in an intracerebroventricular single dose streptozotocin (STZ)-induced Alzheimer model in rats. We arranged 4 groups: Sham and groups receiving STZ and STZ + H-MGL (1 and 2 mg/kg). The H-MGL was administered consecutively for 14 days following the STZ injection. Then, the Morris water maze test was performed. RESULTS: The findings suggest that administration of STZ caused a significantly increment in mean escape latency and mean traveled distance in acquisition days. H-MGL at a 1 mg/kg dosage failed to yield any notable improvement in rats compared to STZ. By contrast, 2 mg/kg of H-MGL dosage led to a significant decrease in the latency to first platform crossing and frequency of platform crossings. CONCLUSION: Consequently, the findings above have engendered the notion that H-MGL partially ameliorates cognitive impairment, so it may hold promise for having low side effects to alleviate cognitive deficits in AD or potentially decrease the symptoms associated with its progression.

特别声明

1、本页面内容包含部分的内容是基于公开信息的合理引用;引用内容仅为补充信息,不代表本站立场。

2、若认为本页面引用内容涉及侵权,请及时与本站联系,我们将第一时间处理。

3、其他媒体/个人如需使用本页面原创内容,需注明“来源:[生知库]”并获得授权;使用引用内容的,需自行联系原作者获得许可。

4、投稿及合作请联系:info@biocloudy.com。