Alatawi_2025_Scientifica.(Cairo)_2025_8209714

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 kappaB (NFkappaB), BCL2-associated X (BAX), tumor necrosis factor-alpha (TNF-alpha), and Interleukin-1 beta (IL-1beta) 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-kappaB, TNF-alpha, and IL-1beta. 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-kappaB, TNF-alpha, and IL-1beta, thereby decreasing cellular apoptosis through the downregulation of BAX and upregulation of BCL-2.