ArticleMolecular medicine reports2018
(‑)Epigallocatechin‑3‑gallate attenuates anesthesia‑induced memory deficit in young mice via modulation of nitric oxide expression.
Article in Molecular medicine reports, 2018. 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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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.
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Who cites it
4 citing papers in PubMed, 10 citations in OpenAlex.
- Role of Dietary Polyphenols in the Activity and Expression of Nitric Oxide Synthases: A Review.Antioxidants (Basel, Switzerland) · 2023Review
- Green Tea, A Medicinal Food with Promising Neurological Benefits.Current neuropharmacology · 2021Review
- (-)-Epigallocatechin-3-gallate provides neuroprotection via AMPK activation against traumatic brain injury in a mouse model.Naunyn-Schmiedeberg's archives of pharmacology · 2020Article
- A Review of the Role of Green Tea (Nutrients · 2019Review
Corrections and comments
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Authors and funding
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
(‑)Epigallocatechin‑3‑gallate (EGCG) is a type of polyphenol monomer and is the predominant component of catechin compounds extractable from green tea. Previous studies have demonstrated that EGCG exhibits numerous bioactivities both in vitro and in vivo, including antitumor, antioxidant and anti‑inflammatory activities, as well as lowering blood lipid levels and protecting against radiation. The present study aimed to investigate whether administration of EGCG may attenuate anesthesia‑induced memory deficit in young mice and to reveal the associated underlying mechanisms. The present study revealed that EGCG administration significantly attenuated memory deficit, oxidative stress and cell apoptosis exhibited by anesthesia‑induced mice, as determined by Morris water maze testing and ELISA analysis. Furthermore, the results of ELISA and western blot analysis demonstrated that EGCG administration restored acetylcholinesterase activity and modulated the expression levels of neuronal nitric oxide synthase (nNOS), β‑amyloid and amyloid precursor protein in anesthesia‑induced mice. The present study also employed L‑arginine as an nNOS substrate and 7‑nitroindazole as an nNOS inhibitor, which were demonstrated to inhibit or potentiate the effects of EGCG, respectively, on anesthesia‑induced memory deficit in mice. Therefore, the present study demonstrated that the administration of EGCG attenuated anesthesia‑induced memory deficit in young mice, potentially via the modulation of nitric oxide expression and oxidative stress.
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