The Potential Protective Effects of EGCG Against Epilepsy-Induced Damage in Rats - by Mitigating Oxidative Stress, Inflammation, and Apoptosis

Sep 30, 2026

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Evaluation of EGCG as a protective agent against epilepsy-induced brain injury in rats was conducted using a pentylenetetrazol (PTZ) model. Animals received 20 mg/kg EGCG, and outcomes included seizure severity and frequency, acetylcholinesterase (AChE) activity, and histological and molecular markers. Brain sections were stained with cresyl violet and anti-Nrf2 immunostaining, while expression and levels of BCL2, Nrf2, NFκB, BAX, TNF-α, and IL-1β were analyzed. EGCG improved behavior, increased Nissl granule staining intensity, upregulated BCL2, Nrf2, and HO-1, and reduced BAX, NFκB, TNF-α, and IL-1β, indicating reduced oxidative stress, inflammation, and apoptosis.

LanguageEnglish

CategoryHealthcare

FormatPDF

Pages13

Reading Time33 min

AccessFree to download

Introduction

Epilepsy background and mechanisms

Treatment options and limitations

Study rationale and approach

EGCG protective effects focus

Wiley Scientifica Volume 2025, Article ID 8209714, 13 pages [https://doi.org/10.1155/sci5/8209714](https://doi.org/10.1155/sci5/8209714) Research Article The Potential Protective Effects of EGCG Against Epilepsy-Induced Damage in Rats by Mitigating Oxidative Stress, Inflammation, and Apoptosis Sarah Alatawi , 1 Manal S. Albalawi , 1 Ruba M. Alfaif , 1 Rand Al-Twalhy , 1 Manal D. Al-Johani , 1 Danah Alanazi , 1 Rinad M. Al-Otaibi , 1 Hanan M. Hassan 2 , and Mohammed M. H. Al-Gayyar 3,4 1 Faculty of Pharmacy, University of Tabuk, Tabuk, Saudi Arabia 2 Department of Pharmacology and Biochemistry, Faculty of Pharmacy, Delta University for Science and Technology, Gamasa City, Egypt 3 Department of Biochemistry, Faculty of Pharmacy, Mansoura University, Mansoura, Egypt 4 Department of Pharmaceutical Chemistry, Faculty of Pharmacy, University of Tabuk, Tabuk, Saudi Arabia Correspondence should be addressed to Mohammed M. H. Al-Gayyar; [mhgayyar@yahoo.com](mhgayyar@yahoo.com) Received 16 October 2025; Revised 19 November 2025; Accepted 3 December 2025 Academic Editor: Tzong-Shyuan Lee Copyright © 2025 Sarah Alatawi et al. Scientifca published by John Wiley & Sons Ltd. Tis is an open access article under the terms of the Creative Commons Attribution License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited. We conducted this study to evaluate the protective efects of Epigallocatechin-3-gallate (EGCG) against epilepsy in rats, with a specifc focus on its potential to mitigate oxidative stress, infammation, and apoptosis. Epilepsy was induced in rats using pentylenetetrazol (PTZ), followed by treatment with 20 mg/kg of EGCG. Te efects of EGCG were assessed on seizure severity and frequency, as well as acetylcholinesterase (AChE) activity. Brain sections were stained with cresyl violet and immune-stained with anti-Nrf2 antibody. Furthermore, expressions and concentrations of B-Cell Lymphoma 2 (BCL2), Nuclear Factor Erythroid 2–Related Factor-2 (Nrf2), nuclear factor κB (NFκB), BCL2-associated X (BAX), tumor necrosis factor-α (TNF-α), and Interleukin-1 β (IL-1β) in brain tissues were analyzed. Rats showed signifcant behavioral improvement following EGCG treatment. Analysis of the dentate gyrus sections demonstrated a modest increase in the staining intensity of Nissl granules after EGCG. Additionally, EGCG was observed to increase the expression levels of BCL2, Nrf2, and Heme Oxygenase-1 (HO-1), while concurrently reducing the expression of BAX, NF-κB, TNF-α, and IL-1β . In conclusion, EGCG demonstrates protective efects against epilepsy. Te underlying mechanisms may be attributed to its capacity to increase antioxidant activity by the upregulation of Nrf2 and HO-1 . EGCG appears to mitigate infammation by downregulating NF-κB, TNF-α, and IL-1β, thereby decreasing cellular apoptosis through the downregulation of BAX and upregulation of BCL-2 . Keywords: acetylcholinesterase (AChE); B-cell lymphoma 2 (BCL2); Bcl-2-associated X protein (BAX); dopamine (DA); heme oxygenase-1 (HO-1); interleukin-1 beta (IL-1β); nuclear factor 2 (Nrf2); nuclear factor kappa B (NF-κB); tumor necrosis factor alpha (TNF-α) 1. Introduction Epilepsy, a neurological disorder, is characterized by recurrent seizures, which arise from sudden, abnormal electrical activity in the brain, leading to transient disruptions in normal brain function. Tese seizures can manifest in diverse forms, such as convulsions, loss of awareness, unusual sensations, and uncontrollable movements [1] . Te mechanisms underlying epilepsy involve the complex interplay of several key neurotransmitters, including serotonin, dopamine, γ-aminobutyric acid (GABA), glutamate, and noradrenaline. Tese neurotransmitters modulate the 2 Scientifca balance of excitation and inhibition in the brain, infuencing the onset and spread of seizures. Symptoms of epilepsy exhibit considerable variability an

FAQs

How was epilepsy induced and how was EGCG administered in the study?

Epilepsy was induced in rats using pentylenetetrazol (PTZ). Rats were treated with 20 mg/kg EGCG after induction.

Which biomarkers and assays were used to assess EGCG’s protective effects?

Seizure severity and frequency, as well as acetylcholinesterase (AChE) activity, were measured. Brain tissue analysis included cresyl violet staining, anti-Nrf2 immunostaining, and evaluation of BCL2, Nrf2, NFκB, BAX, TNF-α, and IL-1β levels and expressions.

What effects did EGCG have on oxidative stress, inflammation, and apoptosis markers?

EGCG increased Nrf2 and HO-1 while upregulating BCL2 and reducing BAX. It also downregulated NFκB, TNF-α, and IL-1β, consistent with reduced inflammation and cellular apoptosis.

Sep 30, 2026

Uploaded by jay