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EGCG Attenuates CA1 Neuronal Death by Regulating GPx1, NF-κB S536 Phosphorylation and Mitochondrial Dynamics in the Rat Hippocampus following Status Epilepticus

Biology

EGCG Attenuates CA1 Neuronal Death by Regulating GPx1, NF-κB S536 Phosphorylation and Mitochondrial Dynamics in the Rat Hippocampus following Status Epilepticus

A. V. Kozlov, S. Javadov, et al.

Discover how epigallocatechin-3-gallate (EGCG) can protect neurons from damage caused by status epilepticus in rats. This innovative research shows that EGCG not only reduces neuronal death but also improves mitochondrial health by modulating critical pathways, revealing exciting potential for neuroprotection. This study was conducted by Andrey V Kozlov, Sabzali Javadov, Natascha Sommer, Ji-Eun Kim, Tae-Hyun Kim, and Tae-Cheon Kang.

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Playback language: English
Abstract
This study investigated the neuroprotective effects of epigallocatechin-3-gallate (EGCG) on CA1 neuronal death following status epilepticus (SE) in rats. EGCG attenuated SE-induced CA1 neuronal death and mitochondrial hyperfusion by upregulating glutathione peroxidase-1 (GPx1), preserving ERK1/2-DRP1-mediated mitochondrial fission, and inhibiting NF-κB S536 phosphorylation. ERK1/2 inhibition blocked EGCG's neuroprotective and mitochondrial effects, suggesting ERK1/2 activation is crucial for EGCG's mechanism.
Publisher
Antioxidants
Published On
Apr 20, 2023
Authors
Andrey V Kozlov, Sabzali Javadov, Natascha Sommer, Ji-Eun Kim, Tae-Hyun Kim, Tae-Cheon Kang
Tags
epigallocatechin-3-gallate
neuroprotection
status epilepticus
neuronal death
mitochondrial fission
glutathione peroxidase-1
ERK1/2

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