THE AMELIORATIVE ANTIOXIDANT EFFECTS OF EGCG ON CORTICO-NEURONAL DAMAGE IN DUAL-INDUCED ALZHEIMER’S DISEASE MODEL USING SWISS WISTAR RATS
Abstract
ABSTRACT
Alzheimer’s disease is a progressive neurodegenerative disorder characterized by cognitive decline, neuronal loss, and increased oxidative stress. This study investigated the ameliorative antioxidant effects of Epigallocatechin Gallate on cortico-neuronal damage in a dual-induced Alzheimer’s disease model using Swiss Wistar rats, with a focus on Superoxide Dismutase activity.
A total of experimental animals were divided into five groups, including a normal control, a negative control, treatment groups receiving low and high doses of EGCG, and a standard drug group. Alzheimer’s disease was induced using a dual-agent method to mimic the multifactorial nature of the disease. EGCG was administered for a specified period, after which brain tissues were analyzed for biochemical and histological changes.
Results showed that dual induction significantly reduced Superoxide Dismutase activity and increased lipid peroxidation, indicating elevated oxidative stress. Histopathological analysis revealed severe cortico-neuronal damage in the untreated group. Treatment with EGCG resulted in a dose-dependent increase in Superoxide Dismutase activity, reduction in oxidative stress markers, and improvement in neuronal structure.
The findings suggest that Epigallocatechin Gallate exerts neuroprotective effects by enhancing antioxidant defense mechanisms and reducing oxidative damage. This study highlights the potential of EGCG as a therapeutic agent in the management of Alzheimer’s disease.
Full-Text Access Notice
In accordance with the NERD Policy on promoting peer-reviewed publication, public access to the full text of a project, thesis or dissertation is restricted for three years, allowing the author and supervisors sufficient time to pursue peer-reviewed publication.
During this period, researchers with legitimate academic or research purposes may request authorisation directly from the author to enable NERD to release the indexed full texts of the work using the form below.