Valeric acid reduction by chitosan oligosaccharide induces autophagy in a Parkinson's disease mouse model

Parkinson's disease (PD) is a central nervous system disease with the highest disability and mortality rate worldwide, and it is caused by a variety of factors. The most common medications for PD have side effects with limited therapeutic outcomes. Many studies have reported that chitosan oligosaccharide (COS) crossed blood-brain barrier to achieve a neuroprotective effect in PD. However, the role of COS in PD remains unclear. The present study demonstrated that COS increased dopaminergic neurons in the substantia nigra (SN) and ameliorated dyskinesia in a PD mouse model. Moreover, COS reduced gut microbial diversity and faecal short-chain fatty acids. Valeric acid supplementation enhanced the inflammatory response in the colon and SN, and it reversed COS - suppressed dopamine neurons damage. Autophagy was involved in COS modulating inflammation through valeric acid. These results suggest that COS reduces bacterial metabolites - valeric acid, which diminishes inflammation via activating autophagy, ultimately alleviating PD.

Medienart:

E-Artikel

Erscheinungsjahr:

2024

Erschienen:

2024

Enthalten in:

Zur Gesamtaufnahme - volume:32

Enthalten in:

Journal of drug targeting - 32(2024), 4 vom: 01. Apr., Seite 423-432

Sprache:

Englisch

Beteiligte Personen:

Chen, Rongsha [VerfasserIn]
Li, Ke [VerfasserIn]
Wang, Yinying [VerfasserIn]
Song, Liyun [VerfasserIn]
Wang, Ruohua [VerfasserIn]
Fan, Wenhui [VerfasserIn]
Zhao, Ninghui [VerfasserIn]
Zou, Wei [VerfasserIn]
Yang, Zhongshan [VerfasserIn]
Yan, Jinyuan [VerfasserIn]

Links:

Volltext

Themen:

9012-76-4
Autophagy
Chitosan
Chitosan oligosaccharide
GZK92PJM7B
Inflammation
Journal Article
N-pentanoic acid
Neuroprotective Agents
Oligosaccharides
Parkinson’s disease
Pentanoic Acids
Valeric acid

Anmerkungen:

Date Completed 03.04.2024

Date Revised 03.04.2024

published: Print-Electronic

Citation Status MEDLINE

doi:

10.1080/1061186X.2024.2315468

funding:

Förderinstitution / Projekttitel:

PPN (Katalog-ID):

NLM368047296