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.