ArticleScientifica2025
The Potential Protective Effects of EGCG Against Epilepsy-Induced Damage in Rats by Mitigating Oxidative Stress, Inflammation, and Apoptosis.
Article in Scientifica, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
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Who cites it
3 citing papers in PubMed.
- Neuroinflammation in Epilepsy: Biochemical and Molecular Mechanisms and Implications for Natural Product-Driven Drug Discovery.International journal of molecular sciences · 2026Review
- Targeting the osteoimmune microenvironment to prevent regulated chondrocyte death in osteoarthritis: therapeutic potential of natural products.Frontiers in cell and developmental biology · 2026Review
- The Potential Protective Effects of EGCG Against Epilepsy-Induced Damage in Rats by Mitigating Oxidative Stress, Inflammation, and Apoptosis.Scientifica · 2025Article
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Authors and funding
9 authors.
Funding
No grant is acknowledged in the PubMed record.
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.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.