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

## TL;DR

This study shows that EGCG may protect against epilepsy in rats by reducing oxidative stress, inflammation, and cell death.

## Contribution

The study reveals EGCG's novel protective mechanisms against epilepsy through modulation of oxidative stress and inflammatory pathways.

## Key findings

- EGCG treatment improved seizure behavior and Nissl staining in rat brain sections.
- EGCG upregulated BCL2, Nrf2, and HO-1 while downregulating BAX, NF-κB, TNF-α, and IL-1β.
- The protective effects of EGCG are linked to reduced oxidative stress and inflammation.

## Abstract

We conducted this study to evaluate the protective effects of Epigallocatechin‐3‐gallate (EGCG) against epilepsy in rats, with a specific focus on its potential to mitigate oxidative stress, inflammation, and apoptosis. Epilepsy was induced in rats using pentylenetetrazol (PTZ), followed by treatment with 20 mg/kg of EGCG. The effects 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 significant 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 effects against epilepsy. The underlying mechanisms may be attributed to its capacity to increase antioxidant activity by the upregulation of Nrf2 and HO‐1. EGCG appears to mitigate inflammation by downregulating NF‐κB, TNF‐α, and IL‐1β, thereby decreasing cellular apoptosis through the downregulation of BAX and upregulation of BCL‐2.