Abstract

There is an increasing link between oxidative stress, inflammation, and neuronal damage in neurodegenerative dis-eases. Therefore, there is the need for safer natural neuroprotective drugs to protect neurons from damage. This study aimed to investigate the neuroprotective effect of natural extracts derived from Olea Europaea plants from Libya. Leaves and fruits of the olives were extracted using ethanol and methanol solvents. The extracts were then analyzed for the presence of phytochemicals and antioxidants, and neuroprotective activity was determined using neuronal cell models. Findings from the study show that olive extract was rich in phenols, flavonoids, oleuropein, and hydroxytryrosol in methanol extracts of leaves. There was a high free radical scavengeing capacity as shown by antioxidant activity tests. Moreover, neuroprotective studies show that the extracts could in-crease neuronal cell viability and reduce intracellular reactive oxygen species when cells are exposed to oxidative stress. Inflammation markers such as TNF-α and IL-6 were also inhibited by the extracts.

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.

Keywords: Ginkgo biloba; Parkinson's disease; ROT treatment; neuroprotection; oxidative stress; rotenone.