Parkinson’s
disease (PD) is the second most common neurodegenerative disease,
frequently associated with a gastric ulcer. We aimed to investigate
the adropin neuroprotective/gastroprotective potential in the indomethacin
(IND)-induced gastric ulcer in a rotenone-induced PD model. Rats were
randomly divided into four groups: normal control group, rotenone/IND
treated (PD /Ulcer) group, adropin treated PD/Ulcer group, and l-dopa/omeprazole (Om) treated PD/Ulcer group. There were ten
rats selected for the normal control group. Striatal dopamine (DA),
apoptosis/redox status, and motor/behavioral impairments were evaluated.
Gastric oxidative stress, H+/K+-ATPase activity,
prostaglandin E2, mucin content, and von Willebrand factor were measured.
Gastric/striatal phosphatidylinositol 3-kinase (PI3K)/phosphorylated
Akt and gastric vascular endothelial growth factor (VEGF)/striatal
P53 immunoreactivities were checked. Striatal P53 upregulated
modulator of apoptosis (Puma)/gastric
vascular endothelial growth factor receptor-2 (Vegfr-2) expressions were evaluated. Adropin successfully restored striatal
DA and attenuated rotenone-induced motor/behavior deficits along with
strong gastroprotective potential, possibly through antioxidant activity
via reduction in malondialdehyde level and upregulated superoxide
dismutase, catalase activities, and serum ferric reducing antioxidant
power. Adropin restored the delicate balance between the defective
pro-survival PI3K/Akt/murine double minute 2 signals and apoptotic
P53/Puma pathways. Adropin can be considered as a
uniquely attractive therapeutic target in PD and its associated gastric
ulcer.
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