{"id":"6c5f5c57-da74-47bf-8bae-1e837ac2d39b","slug":"sni-17-530","title":"Neuroprotective effects of oleuropein on dopamine level and caspase-3 activity in zebrafish model of Parkinson’s disease","authors":["Tommy Rizky Hutagalung","Kiking Ritarwan","Sabri Ibrahim","Cut Aria Arina","Achmad Fahmi","Aida Fitri","Mustafa Mahmud Amin","Mutiara Indah Sari"],"abstract":"Background: Parkinson’s disease (PD) is characterized by the progressive loss of dopaminergic neurons in the substantia nigra, largely driven by oxidative stress-mediated apoptosis. Caspase-3 acts as the central executioner in this cell death pathway. While oleuropein, a phenolic compound fromOlea europaea, is known for its antioxidant properties, its specific mechanism in modulating the caspase-3-dopamine axis inin vivoPD models remains to be fully elucidated. This study aimed to investigate the neuroprotective and neurorestorative effects of oleuropein isolate on brain dopamine levels and caspase-3 activity in a Rotenone-induced zebrafish (Danio rerio) model of PD. Methods: Thirty adult male zebrafish were randomized into five groups: Negative control, positive control (Rotenone induced), and three treatment groups (preventive, curative, and co-treatment) receiving oleuropein isolate (100 mg/kg). The PD model was established through rotenone induction to trigger mitochondrial dysfunction. Brain tissues were analyzed using specific enzyme-linked immunosorbent assay kits to quantify dopamine concentrations and caspase-3 activity. Data were analyzed using one-way analysis of variance followed by Tukey’spost hoctest. Results: Rotenone induction significantly elevated caspase-3 activity (29.74 ± 0.93 ng/mL) and depleted dopamine levels (20.67 ± 0.79 ng/mL) compared to controls (p< 0.05), confirming apoptotic neurodegeneration. Oleuropein administration significantly reversed these pathological changes across all protocols (p< 0.001). The co-treatment group exhibited the most potent suppression of caspase-3 (23.22 ± 0.50 ng/mL), while the curative group demonstrated the highest restoration of dopamine levels (25.31 ± 0.53 ng/mL), suggesting a compensatory neurorestorative mechanism. Conclusion: Oleuropein effectively mitigates dopaminergic neurodegeneration by inhibiting caspase-3-mediated apoptosis, which directly correlates with the functional restoration of brain dopamine levels. These findings support the potential of oleuropein as a therapeutic agent for preventing neuronal death and restoring dopaminergic function in PD.","thumbnailUrl":"https://sni-digital-videos.s3.amazonaws.com/articles/sni-17-530/figures/SNI-17-530-g001.jpg","publishDate":"2026-09-18T00:00:00.000Z","doi":"10.25259/SNI_922_2026","categories":["Neuroanatomy and Neurophysiology","Original Article"],"fullTextUrl":"https://surgicalneurologyint.com/api/articles/6c5f5c57-da74-47bf-8bae-1e837ac2d39b/pdf"}