THE AMELIORATIVE ANTI- INFLAMMATORY EFFECTS OF EGCG ON THE EXPRESSION OF NEUROINFLAMMATORY MARKERS IN DUAL-INDUCED ALZHEIMER’S DISEASE MODEL USING SWISS WISTAR RATS. (NF-ΚB AND GFAP)
Abstract
Alzheimer’s disease (AD) is a progressive neurodegenerative disorder characterized by cognitive decline, neuronal degeneration, oxidative stress, and chronic neuroinflammation. Neuroinflammatory processes mediated by glial activation and inflammatory signaling pathways, particularly Nuclear Factor-kappa B (NF-κB) and Glial Fibrillary Acidic Protein (GFAP), have been implicated in the pathogenesis and progression of AD. Epigallocatechin-3-gallate (EGCG), a major polyphenolic compound found in green tea, possesses potent antioxidant and anti-inflammatory properties that may offer neuroprotective benefits against AD-related neurodegeneration. This study investigated the ameliorative anti-inflammatory effects of EGCG on the expression of neuroinflammatory markers in a dual-induced Alzheimer’s disease model using Swiss Wistar rats.
Adult Swiss Wistar rats were randomly assigned into experimental groups, including normal control, Alzheimer’s disease-induced control, and treatment groups administered varying doses of EGCG following dual induction of AD. Alzheimer-like pathology was induced using combined neurotoxic agents to mimic cognitive impairment and neuroinflammatory alterations associated with the disease. Following treatment, brain tissues were harvested and analyzed for the expression of NF-κB and GFAP using standard histological and immunohistochemical techniques.
Results revealed a significant upregulation of NF-κB and GFAP expression in the AD-induced group compared to the normal control, indicating enhanced neuroinflammatory activity and astrocytic activation. However, administration of EGCG significantly reduced the expression levels of these neuroinflammatory markers in treated groups when compared with the untreated AD group. The reduction in NF-κB and GFAP expression suggests that EGCG attenuated inflammatory responses and glial activation in the brain tissues of the experimental animals.
The findings of this study demonstrate that EGCG exerts ameliorative anti-inflammatory effects against neuroinflammation in dual-induced Alzheimer’s disease models. Its neuroprotective potential may be linked to the suppression of inflammatory signaling pathways and reduction of astrocyte reactivity. Therefore, EGCG may represent a promising therapeutic candidate for the management and prevention of neuroinflammatory changes associated with Alzheimer’s disease.
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