Hippocampal GDNF signaling modulation by high-intensity interval swimming and gallic acid in an animal model of Parkinson's disease.
Hippocampal GDNF signaling modulation by high-intensity interval swimming and gallic acid in an animal model of Parkinson's disease.
Where did the research take place?
The study site has not been established. Author addresses may differ from where the research occurred.
Shiraz, IR · Author affiliation
Department of Physical Education, Shi.C., Islamic Azad University, Shiraz, Iran.Location evidence
Jahrom, IR · Author affiliation
Department of Physical Education, Jah.C., Islamic Azad University, Jahrom, Iran.Location evidence
Chicago, US · Author affiliation
Department of Kinesiology and Nutrition, University of Illinois Chicago, Chicago, IL, USA.Location evidence
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Original abstract
OBJECTIVE: Neurotrophic signaling is dysregulated in Parkinson's disease (PD), while gallic acid possesses anti-inflammatory and potential neuroprotective properties. This study investigated the effects of high-intensity interval training (HIIT) swimming and gallic acid supplementation on the glial cell line-derived neurotrophic factor (GDNF) signaling pathway in a rat model of PD. MATERIALS AND METHODS: Thirty-five male Wistar rats (8-10 weeks) were randomly assigned to five groups: healthy control, PD control, PD + HIIT swimming, PD + gallic acid, and PD + HIIT + gallic acid. PD was induced by reserpine (1 mg/kg/day, 5 days). Following induction, animals underwent six weeks of HIIT swimming (three sessions/week), while supplemented groups received gallic acid (200 mg/kg, three times/week). Gene expression levels of GDNF, RET proto-oncogene (RET), nuclear receptor-related 1 protein (NURR1), and microRNA-132 (miR-132) were assessed in hippocampal tissue. RESULTS: Reserpine significantly reduced GDNF (p = 0.003), RET (p = 0.03), and NURR1 (p = 0.04) expression and increased miR-132 expression (p = 0.002) compared with healthy controls. HIIT increased GDNF (p = 0.002), RET (p = 0.001), and NURR1 (p = 0.01) expression and decreased miR-132 expression (p = 0.04). Gallic acid significantly affected RET expression (p = 0.02), whereas its effects on GDNF (p = 0.05), NURR1 (p = 0.07), and miR-132 (p = 0.16) were not significant. No significant interaction was observed between HIIT and gallic acid for GDNF (p = 0.11), RET (p = 0.86), NURR1 (p = 0.08), or miR-132 (p = 0.83). CONCLUSION: HIIT swimming effectively modulated components of the GDNF signaling pathway in this PD model, suggesting its neuroprotective potential. Gallic acid did not provide additional benefits under these conditions, and HIIT swimming showed broader effects than gallic acid.