Objective: This study aimed to investigate the neuroprotective potential of thymol in an MPTP-induced Parkinson’s disease (PD) model in rats, focusing on its ability to mitigate dopaminergic (DA) neuron degeneration, oxidative stress, mitochondrial dysfunction, and neuroinflammation through behavioral, biochemical, and molecular approaches.

Background: Parkinson’s disease (PD) is a progressive neurodegenerative disorder marked by the selective loss of DA neurons in the substantia nigra pars compacta, resulting in motor dysfunction and cognitive decline. MPTP, a neurotoxin, mimics PD pathology by inducing mitochondrial dysfunction, oxidative stress, and neuroinflammation, ultimately leading to DA neuron degeneration. Thymol, a monoterpene phenol, exhibits antioxidant, anti-inflammatory, and neuroprotective properties, which may counteract the pathophysiological mechanisms underlying PD.

Method: Adult male Wistar rats were divided into four groups: control, MPTP (30 mg/kg, i.p.), thymol (50 mg/kg, oral), and MPTP + thymol administration. Behavioral assessments included rotarod, open field, and grip strength tests to evaluate motor coordination and activity. Oxidative stress markers (MDA, SOD, CAT, GSH) and mitochondrial enzyme activity (complex I-IV) were measured using spectrophotometric assays. Inflammatory markers (TNF-α, IL-6, and IL-1β) were quantified using ELISA. Immunohistochemistry was used to assess DA neuron integrity in the substantia nigra. Molecular docking analysis was conducted to evaluate thymol’s binding affinity with DA-related targets, including monoamine oxidase B (MAO-B) and tyrosine hydroxylase.

Results: MPTP administration significantly impaired motor function, increased oxidative stress, and reduced TH expression in the substantia nigra. Thymol co-treatment restored motor deficits, reduced oxidative stress, suppressed inflammatory cytokine levels, and improved mitochondrial enzyme activity. Molecular docking revealed strong binding affinity of thymol with MAO-B and TH, suggesting a direct neuroprotective mechanism.

Conclusion: Thymol demonstrated significant neuroprotection in the MPTP-induced PD model by preserving DA neuron integrity, enhancing mitochondrial function, and reducing oxidative stress and inflammation. These findings support the potential of thymol as a therapeutic agent for Parkinson’s disease.

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MDS Abstracts - https://www.mdsabstracts.org/abstract/neuroprotective-effects-of-thymol-in-mptp-induced-parkinsons-disease-model-in-rats-molecular-docking-behavioral-biochemical-and-histological-investigations/