Edaravone Protects Nerve Synapse Damage in Alzheimer’s Disease via Regulating Rho (Ras Homologue)/Rho-Associated Protein Kinase (Rho/ROCK) Pathway
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Published:2021-07-01
Issue:7
Volume:11
Page:1352-1357
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ISSN:2157-9083
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Container-title:Journal of Biomaterials and Tissue Engineering
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language:en
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Short-container-title:j biomater tissue eng
Author:
Zhang Shan-Jing1,
Ni Jian-Ming1,
Ding Guo-Rong1,
Xie Yan-Zhong1,
Tang Yan-Liang1
Affiliation:
1. Department of Internal Medicine, Hangzhou Fuyang Hospital of Traditional Chinese Medicine, Hangzhou, Zhejiang 311400, China
Abstract
Edaravone regulates Rho/ROCK signaling pathway and its relationship with Alzheimer’s disease (AD) damage repair remains unclear. Our study aims to explore the protective mechanism of edar-avone on Alzheimer Disease nerve synapses. The Alzheimer Disease animal mouse model was established
followed by analysis of hippocampal synaptic damage by Congo red stain and Golgi’s method, Morris water maze assay, levels of postsynaptic density mRNA 95 antibody (PSD95) and synapse-associated mRNA synapsin 1 (SYN1) in the hippocampus. Edaravone can improve the behavior of mice, including
spatial learning and memory, and reduce senile plaques in the cerebral cortex of APP/PS1 mice. Edaravone can upregulate the expression of synapse-related mRNA SYN1 and PSD95 in the hippocampus of APP/PS1 mice and inhibit Rho and ROCK mRNA level. Edaravone targets the Rho/ROCK pathway to protect
Alzheimer Disease nerve synapse damage, indicating that the Rho/ROCK pathway may be a key link in the effect of edaravone.
Publisher
American Scientific Publishers
Subject
Biomedical Engineering,Medicine (miscellaneous),Bioengineering,Biotechnology