Naitian Wang,
Duohui Liu,
Xinyu Ning,
Zhanjun Li,
Lan Dong
The People's Liberation Army General Hospital Center, Beijing, China;
For correspondence:- Lan Dong
Email: xing217312@163.com Tel:+8613723142517
Accepted: 26 April 2020
Published: 30 December 2020
Citation:
Wang N, Liu D, Ning X, Li Z, Dong L.
CS nerve growth factor regulates sevoflurane anesthesia-induced nerve injury in nerve cells. Trop J Pharm Res 2020; 19(12):2529-2536
doi:
10.4314/tjpr.v19i12.7
© 2020 The authors.
This is an Open Access article that uses a funding model which does not charge readers or their institutions for access and distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0) and the Budapest Open Access Initiative (http://www.budapestopenaccessinitiative.org/read), which permit unrestricted use, distribution, and reproduction in any medium, provided the original work is properly credited..
Abstract
Purpose: Sevoflurane is the most commonly used anesthetic agent for surgery. However, it is associated with deficiency in learning and memory abilities. The study was aimed at investigating the role of nerve growth factor (NGF) in sevoflurane anesthesia-induced nerve injury.
Methods: RT-qPCR assay was applied to measure expressions of NGF, miR-98-5p and other factors related to apoptosis. CCK-8 assay was used for detecting cell viability while luciferase reporter assay was employed to measure binding condition between miR-98-5p and NGF. expressions of proteins in PI3K/AKT/mTOR signaling pathway was measured with western blot.
Results: Sevoflurane reduced cell viability of RGC-5 cells, promoted apoptosis and reduced the expression of NGF. In sevoflurane-induced RGC-5 cells, over-expression of NGF promoted cell viability with reduced apoptosis. Also, there was reduction in the protein expression of PI3K/AKT/mTOR signaling pathway by sevoflurane, while up-regulation of NGF promoted the expressions of these proteins. In the presence of PI3K inhibitor, reduction cell viability was reduced but apoptosis increased. Luciferase reporter assay detected MiR-98-5p as the target gene of NGF and its overexpression restored high cell viability in the over-expressed NGF. The rate of apoptosis and expressions of proteins was also restored with up-regulation of miR-98-5p.
Conclusion: Sevoflurane caused damage to nerve cells, while over-expression of NGF reduced the injury through PI3K/AKT/mTOR signaling pathway and suppression of miR-98-5p.
Keywords: Nerve growth factor, Sevoflurane, Nerve injury, Anesthesia, miR-98-5p