Adropin exerts neuroprotection in an experimental rat model of Parkinson’s disease

TL;DR

Adropin protects brain cells in a rat model of Parkinson's disease by boosting dopamine levels and activating a specific signaling pathway.

Contribution

This study identifies adropin's neuroprotective role in Parkinson’s disease via VEGFR2 signaling and dopamine preservation.

Findings

Adropin improved motor performance and protected dopaminergic neurons in Parkinson's rats.

Adropin increased dopamine levels and activated VEGFR2 in the substantia nigra.

Adropin's effect was not linked to changes in GPR19 or GSK3β phosphorylation.

Abstract

This study was planned to elucidate the mechanism of the protective effect of adropin in an experimental rat model of Parkinson’s Disease (PD).

Three-month-old male Wistar rats were randomly divided into four groups: i) Control, ii) Sham, iii) PD, and iv) PD+Adropin. The performance tests were performed seven days after the 6-Hydroxydopamine hydrochloride (6-OHDA) injection into the striatum. The immunoreactivities for tyrosine hydroxylase (TH), G protein-coupled receptor 19 (GPR19), and vascular endothelial growth factor receptor 2 (VEGFR2) were detected by immunohistochemistry (IHC) in the substantia nigra (SN). Dopamine levels were measured by mass spectrometry. Glycogen synthase kinase 3β (GSK3β) and pGSK3β (Ser9) protein levels were evaluated by western blot analysis.

Our study demonstrated that motor performances were significantly improved by adropin treatment. Central adropin injection prevented the loss of nigral dopaminergic neurons and induced VEGFR2 expression but not GPR19 compared to the PD group. The ratio of p-GSK3β/GSK3β did not differ between groups. However, the level of dopamine in SN was increased with adropin injection in the PD+Adropin group.

Our findings reveal that adropin administration has a protective effect on nigral dopaminergic neurons and acts through the VEGFR2 signaling pathway.

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