Remission effect of vitamin C on isoflurane-induced apoptosis and its mechanism

J. Hu, BF. Gao, HQ. Li, ZZ. Zhang, YL. Lei, GQ. Sun, DM. Guo

Article ID: 4272
Vol 30, Issue 4, 2016
DOI: https://doi.org/10.54517/jbrha4272
Received: 6 June 2022; Accepted: 6 June 2022; Available online: 6 June 2022; Issue release: 6 June 2022

Abstract

This study aims to discuss the remission effect of vitamin C on isoflurane-induced apoptosis of rats and its possible mechanism of action, to provide a theoretical basis for postoperative cognitive impairment. Reactive oxygen species (ROS) detection, adenosine triphosphate (ATP) test, MTT method and Morris water maze were applied for detection tests. For data statistics, double factor analysis of variance (ANOVA) and post hoc Bonferroni test were adopted. It was found that vitamin C could slow down the isoflurane-induced accumulation of ROS in H4-APP cells; moreover, it could relieve the activation of caspase-3 and increase cell survival rate to inhibit the occurrence of apoptosis, indicating that ROS was the source of cell toxicity. On the other hand, vitamin C could protect the cells with its antioxidant effect. It was proved that vitamin C could remit isoflurane-induced apoptosis and relieve the decline in learning and memory ability of rats.


Keywords

vitamin C;cognitive impairment;isoflurane;apoptosis


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Supporting Agencies



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