Synthesis of Novel Magnetic Quercetin-Neuropeptide Nanocomposite as a Smart Nano-Drug Shuttle System: Investigation of Its Effect on Behavior, Histopathological Characteristics, and Expression of MAPT and APP Genes in Alzheimer’s Disease Rats

药理学 海马体 超氧化物歧化酶 神经退行性变 医学 组织病理学 海马结构 槲皮素 内科学 化学 病理 生物化学 疾病 氧化应激 抗氧化剂
作者
Kamelia Mobasheri,Mohammad Zaefizadeh,Maryam Ghobeh,Akram Eidi
出处
期刊:Journal of Alzheimer's Disease [IOS Press]
卷期号:94 (3): 1145-1155
标识
DOI:10.3233/jad-221095
摘要

Background: Alzheimer’s disease (AD) is the most common type of dementia. The drugs introduced for this disease have many side effects and limitations in use, so the production of a suitable herbal medicine to cure AD patients is essential. Objective: The aim of this research is to make a magnetic neuropeptide nano shuttle as a targeted carrier for the transfer of quercetin to the brains of AD model rats. Methods: In this work, a magnetic quercetin-neuropeptide nanocomposite (MQNPN) was fabricated and administered to the rat’s brain by the shuttle drug of the Margatoxin scorpion venom neuropeptide, and will be a prospect for targeted drug delivery in AD. The MQNPN has been characterized by FTIR, spectroscopy, FE-SEM, XRD, and VSM. Investigations into the efficacy of MQNPN, MTT, and real Time PCR for MAPT and APP genes expression were performed. After 7 days treatment with Fe3O4 (Ctr) and MQNPN treatment in AD rat, superoxide dismutase activity and quercetin in blood serum and brain was detected. Hematoxylin-Eosin staining was applied for histopathological analysis. Results: Analysis of data showed that MQNPN increased the activity of superoxide dismutase. The histopathology results of the hippocampal region of AD rats also confirmed their improvement after treatment with MQNPN. MQNPN treatment caused a significant decrease in the relative expression of MAPT and APP genes. Conclusion: MQNPN is a suitable carrier for the transfer of quercetin to the rat hippocampus, and has a significant effect in reducing AD symptoms in terms of histopathology, behavioral testing, and changing the expression of AD-related genes.
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