ArticleFood science & nutrition2024
Epicatechin-mediated modulation of the Nrf2/HO-1 pathway alleviates senile cerebral ischemic/reperfusion injury.
Article in Food science & nutrition, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed.
- The Role of Nuclear Factor Erythroid 2-Related Factor 2 in the Crosstalk Between Oxidative Stress and M1/M2 Microglial Polarization Following Ischemic Stroke.Molecular neurobiology · 2026Review
- Epicatechin Protects Against Post-Cardiac Arrest Brain Injury in Aged Rats via NRG1-Mediated Suppression of Neuroinflammation.Current issues in molecular biology · 2025Article
- Olfactory mucosa-mesenchymal stem cells with overexpressed Nrf2 modulate angiogenesis and exert anti-inflammation effect in an in vitro traumatic brain injury model.European journal of medical research · 2025Article
- Neuronal Injury after Ischemic Stroke: Mechanisms of Crosstalk Involving Necroptosis.Journal of molecular neuroscience : MN · 2025Review
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6 authors.
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Abstract
Excessive reactive oxygen species (ROS) generated during cerebral ischemic reperfusion (CIRI) are crucial for subsequent tissue damage. However, despite the potential benefits of antioxidants reported in clinical applications, few have proven effective in treating CIRI, particularly in the elderly. Epicatechin (EC) is a catechol flavonoid monomer derived from natural tea plants. Multiple phenolic hydroxyl groups give it strong antioxidant properties, which can not only degrade ROS through chemical reactions between hydroxyl and ROS but also enhance the activity of antioxidant enzymes in cells, and it is easy to penetrate the blood-brain barrier. But its antagonistic effect on age-related CIRI and potential medicinal value are still unknown. Nuclear factor erythroid 2-related factor 2 (Nrf2) is the most important transcription factor regulating the expression of antioxidant proteins in the body. This study first compared the pathological differences of the Nrf2 system in CIRI between 2-month-old and 12-month-old Sprague-Dawley (SD) rats. Subsequently, EC was administered to 12-month-old rat models of middle cerebral artery occlusion and reperfusion (MCAO/R) and senescent SH-SY5Y cell models subjected to oxygen glucose deprivation/reoxygenation (OGD/R). EC treatment improved cerebral morphology and function; increased p-Nrf2, heme oxygenase-1 (HO-1), superoxide dismutase (SOD), and glutathione (GSH) expression; reduced infarct volume; and neuronal apoptosis in senescent rats. Moreover, EC enhanced cellular activity and the expression of p-Nrf2, HO-1, and quinone oxidoreductase-1 (NQO-1) while decreasing ROS and malondialdehyde (MDA) levels and mitigating apoptosis in senescent SH-SY5Y cells. These effects were reversed upon si-Nrf2. In sum, we confirm that EC exerts neuroprotective effects by upregulating Nrf2/ARE and reducing oxidative stress, suggesting that EC may be a promising drug for the treatment of senile cerebral apoplexy. This study also provides a scientific basis for the development and selection of new drugs for ischemic stroke in elderly patients.
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