Neuroprotective effects of idebenone combined with borneol via the dopamine signaling pathway in a transgenic zebrafish model of Parkinson's disease.
10.7507/1001-5515.202401034
- Author:
Qifei WANG
1
;
Yayun ZHONG
1
;
Yanan YANG
1
;
Kechun LIU
1
;
Li LIU
2
;
Yun ZHANG
1
Author Information
1. Biology Institute, Qilu University of Technology (Shandong Academy of Sciences), Jinan 250103, P. R. China.
2. School of Medical and Health Engineering, Changzhou University, Changzhou, Jiangsu 213164, P. R. China.
- Publication Type:Journal Article
- Keywords:
Borneol;
Dopamine signaling pathway;
Idebenone;
Parkinson’s disease;
Transgenic zebrafish
- MeSH:
Animals;
Zebrafish;
Signal Transduction/drug effects*;
Animals, Genetically Modified;
Dopamine/metabolism*;
Neuroprotective Agents/pharmacology*;
Disease Models, Animal;
Camphanes/pharmacology*;
Ubiquinone/pharmacology*;
Parkinson Disease/drug therapy*;
Dopaminergic Neurons/metabolism*
- From:
Journal of Biomedical Engineering
2025;42(5):1046-1053
- CountryChina
- Language:Chinese
-
Abstract:
The aim of this study is to investigate the protective effect of idebenone (IDE) combined with borneol (BO) against Parkinson's disease (PD). In this study, wild-type AB zebrafish and transgenic Tg ( vmat2: GFP) zebrafish with green fluorescence labeled dopamine neurons were used to establish the PD model with 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine hydrochloride (MPTP). Following drug treatment, the behavioral performance and dopamine neuron morphology of zebrafish were evaluated, and regulation of dopamine signaling pathway-related genes was determined using RT-qPCR. The results showed that IDE combined with BO improved the behavioral disorders of zebrafish such as bradykinesia and shortening movement distance, also effectively reversed the damage of MPTP-induced dopaminergic neurons. At the same time, the expression of dopamine synthesis and transportation-related genes was up-regulated, and the normal function of the signal transduction pathway was restored. The combination showed a better therapeutic effect compared to the IDE monotherapy group. This study reveals the protective mechanism of IDE combined with BO on the central nervous system for the first time, which provides an important experimental basis and theoretical reference for clinical combination strategy in PD treatment.
