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1- Neurosciences Research Center, Tabriz University of Medical Sciences, Tabriz, Iran.
2- Department of Pathobiology, Faculty of Veterinary Medicine, Tabriz Medical Sciences, Islamic Azad University, Tabriz, Iran.
3- Department of Basic Sciences, Faculty of Veterinary Medicine, Tabriz Medical Sciences, Islamic Azad University, Tabriz, Iran.
Abstract:  
Neurotrophic factors and physical activities have beneficial effects on neurodegenerative disorders. This study assessed the effect of physical activity (EXE) and Cerebrolysin (CBL), individually or in conjunction, in a hemiparkinsonian model (PD) caused by 6-hydroxydopamine (6-OHDA). The study utilized seventy-two male Wistar rats, which were distributed into six groups (n=12): Sham (received intra substantia nigra (SN) injection of normal saline), PD (underwent 6-OHDA (12.5 μg) injection into the left SN), PD+Levodopa (treated with levodopa; 12 mg/kg, gavage, for three weeks), PD+CBL (treated with intraperitoneal injection of CBL 2.5 ml/kg, for three weeks), PD+EXE (exercised 30 min/day for three weeks), and PD+CBL+EXE. Rotation with apomorphine and Murprogo’s test were assessed, 21 days after PD induction and after treatments. Ultimately, the levels of lipid peroxidation marker and total antioxidant capacity (TAC), glutathione peroxidase (GPx) activity, α-synuclein protein expression, and histopathological changes of the SN were evaluated ipsilateral to the lesioned side. The results showed that CBL and exercise, alone or in combination, decreased ipsilateral apomorphine rotation and muscle rigidity in the PD animals. Moreover, these behavioral changes were associated with decreased malondialdehyde levels and α-synuclein protein levels, increased TAC level and GPx activity, as well as a greater neuronal count in the SN. Notably, the combination effects were greater than single therapy and levodopa treatment. Our findings indicated that the combination of exercise and CBL ameliorated 6-OHDA-induced motor impairments by attenuating oxidative stress and protein expression of α-synuclein, and preserving neurons in the SN.
Type of Study: Original | Subject: Cellular and molecular Neuroscience
Received: 2024/03/3 | Accepted: 2024/11/27

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