Title:Oral Supplements of Ginkgo biloba Extract Alleviate Neuroinflammation, Oxidative Impairments and Neurotoxicity in Rotenone-Induced Parkinsonian Rats
Volume: 21
Issue: 12
Author(s): Nema A. Mohammed, Heba M. Abdou, Mona A. Tass, Manal Alfwuaires, Ashraf M. Abdel-Moneim and Amina E. Essawy*
Affiliation:
- Department of Zoology, Faculty of Science, Alexandria University, Alexandria,Egypt
Keywords:
Ginkgo biloba, neuroprotection, oxidative stress, rotenone, Parkinson's disease, ROT treatment.
Abstract:
Background: Ginkgo biloba extract (GbE) is known to contain several bioactive compounds
and exhibits free radical scavenging activity. Parkinson's Disease (PD) is a neurodegenerative
disorder characterized by the loss of dopaminergic neurons and is associated with oxidative stress, neuroinflammation
and apoptosis.
Objective: The current study aimed to investigate the neuroprotective effect of GbE in a rat model of
PD induced by rotenone (ROT; a neurotoxin).
Methods: Twenty-four male albino rats were randomly divided into four groups of six rats each: normal
control, GbE treated, toxin control (ROT treated) and GbE+ROT group.
Results: Oral administration of ROT (2.5 mg/kg b.w.) for 50 days caused an increased generation of
lipid peroxidation products and significant depletion of reduced glutathione, total thiol content and activities
of enzymatic antioxidants, i.e., superoxide dismutase and glutathione peroxidase in the brains
of treated rats. Furthermore, ROT caused an elevation in acetylcholinesterase, interleukin-1β, interleukin-
6 and tumor necrosis factor-α and a significant reduction in dopamine in the stratum and substantia
nigra. Immunohistochemical results illustrated that ROT treatment reduced the expression of tyrosine
hydroxylase (TH). GbE treatment (150 mg/kg b.w./day) significantly reduced the elevated oxidative
stress markers and proinflammatory cytokines and restored the reduced antioxidant enzyme activities,
DA level and TH expression. These results were confirmed by histological observations that clearly
indicated a neuroprotective effect of GbE against ROT-induced PD.
Conclusion: GbE mitigated ROT-induced PD via the inhibition of free-radical production, scavenging
of ROS, and antioxidant enhancement.
