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1- Department of Biochemistry, Faculty of Medicine, Baqiyatallah University of Medical Sciences, Tehran, Iran
2- Neuroscience Research Center, Baqiyatallah University of Medical Sciences, Tehran, Iran
2- Neuroscience Research Center, Baqiyatallah University of Medical Sciences, Tehran, Iran
Abstract:
Purpose: Parkinson’s disease (PD) is a progressive neurodegenerative disorder and the second most prevalent neurological condition worldwide. Deep Brain Stimulation (DBS) targeting the subthalamic nucleus (STN) has emerged as a contemporary therapeutic approach, demonstrating efficacy in alleviating PD symptoms. This study aimed to examine the effects of STN-DBS on behavioral abnormalities and serum levels of inflammatory and oxidative stress biomarkers in a rat model of PD.
Methods: PD was induced in Wistar rats through administration of the neurotoxin 6-hydroxydopamine (6-OHDA). The animals were then randomly assigned to five groups, each consisting of eight rats: Group 1 (Normal) served as healthy controls without any intervention; Group 2 (PD group) included PD model rats implanted with electrodes but not subjected to DBS; Groups 3 to 5 comprised PD model rats receiving one hour of subthalamic nucleus DBS (STN-DBS) daily for three consecutive days, targeting the right hemisphere, left hemisphere, and bilateral hemispheres, respectively. Three weeks after 6-OHDA treatment, DBS was administered to Groups 3 through 5, followed by behavioral assessments using the Bar test for catalepsy and the Rotarod test for motor coordination. Upon completion of behavioral testing, serum samples were collected to quantify inflammatory markers and oxidative stress parameters via enzyme-linked immunosorbent assay (ELISA) and photometric assays, respectively.
Results: The 6-OHDA lesion induced significant behavioral deficits, which were ameliorated by STN-DBS. Compared to the normal group, the PD group exhibited significantly elevated serum levels of malondialdehyde (MDA), tumor necrosis factor-alpha (TNF-α), interleukin-6 (IL-6), and catalase (CAT) activity (p < 0.001), alongside reductions in reduced glutathione (GSH) and superoxide dismutase (SOD) levels (p < 0.001). In the DBS-treated groups, MDA, TNF-α, and IL-6 concentrations were significantly decreased relative to the PD group (p < 0.001), while GSH levels were significantly increased (p < 0.05 to p < 0.01). Additionally, CAT activity was significantly reduced in all DBS groups (p < 0.01), and SOD activity was significantly elevated in the left hemisphere and bilateral DBS groups compared to the PD group (p < 0.001 and p < 0.05, respectively). Bilateral stimulation had a greater effect on motor coordination and catalepsy than stimulation of the right or left hemisphere. In contrast, the impact of bilateral stimulation on inflammatory factors and oxidative stress markers was not greater than that of unilateral stimulation.
Conclusion: These findings indicate that STN-DBS mitigates behavioral impairments and modulates markers of inflammation and oxidative stress in the 6-OHDA-induced rat model of PD, suggesting its therapeutic potential for managing PD-related pathophysiology.
Methods: PD was induced in Wistar rats through administration of the neurotoxin 6-hydroxydopamine (6-OHDA). The animals were then randomly assigned to five groups, each consisting of eight rats: Group 1 (Normal) served as healthy controls without any intervention; Group 2 (PD group) included PD model rats implanted with electrodes but not subjected to DBS; Groups 3 to 5 comprised PD model rats receiving one hour of subthalamic nucleus DBS (STN-DBS) daily for three consecutive days, targeting the right hemisphere, left hemisphere, and bilateral hemispheres, respectively. Three weeks after 6-OHDA treatment, DBS was administered to Groups 3 through 5, followed by behavioral assessments using the Bar test for catalepsy and the Rotarod test for motor coordination. Upon completion of behavioral testing, serum samples were collected to quantify inflammatory markers and oxidative stress parameters via enzyme-linked immunosorbent assay (ELISA) and photometric assays, respectively.
Results: The 6-OHDA lesion induced significant behavioral deficits, which were ameliorated by STN-DBS. Compared to the normal group, the PD group exhibited significantly elevated serum levels of malondialdehyde (MDA), tumor necrosis factor-alpha (TNF-α), interleukin-6 (IL-6), and catalase (CAT) activity (p < 0.001), alongside reductions in reduced glutathione (GSH) and superoxide dismutase (SOD) levels (p < 0.001). In the DBS-treated groups, MDA, TNF-α, and IL-6 concentrations were significantly decreased relative to the PD group (p < 0.001), while GSH levels were significantly increased (p < 0.05 to p < 0.01). Additionally, CAT activity was significantly reduced in all DBS groups (p < 0.01), and SOD activity was significantly elevated in the left hemisphere and bilateral DBS groups compared to the PD group (p < 0.001 and p < 0.05, respectively). Bilateral stimulation had a greater effect on motor coordination and catalepsy than stimulation of the right or left hemisphere. In contrast, the impact of bilateral stimulation on inflammatory factors and oxidative stress markers was not greater than that of unilateral stimulation.
Conclusion: These findings indicate that STN-DBS mitigates behavioral impairments and modulates markers of inflammation and oxidative stress in the 6-OHDA-induced rat model of PD, suggesting its therapeutic potential for managing PD-related pathophysiology.
Keywords: Parkinson's Disease, 6-OHDA, Deep Brain Stimulation, Inflammatory Biomarkers, Oxidative Stress
Type of Study: Original |
Subject:
Behavioral Neuroscience
Received: 2026/04/12 | Accepted: 2026/05/4
Received: 2026/04/12 | Accepted: 2026/05/4
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