Tropical Journal of Pharmaceutical Research

Original Research Article | OPEN ACCESS

NR4A1 alleviates the toxicity in neural stem cells induced by propofol in early life by regulating AMPK pathway

Miaomiao Zhu, Jing Hu , Baofeng Gao, Changlin Liu, Huiqing Li, Zengzhen Zhang

Department of Anesthesiology, Shandong Provincial Third Hospital, Jinan, Shandong Province 250031, China;

For correspondence:- Jing Hu Email: jhu4376@163.com Tel:+86053181656166

Accepted: 31 January 2023 Published: 27 February 2023

Citation: Zhu M, Hu J, Gao B, Liu C, Li H, Zhang Z. NR4A1 alleviates the toxicity in neural stem cells induced by propofol in early life by regulating AMPK pathway. Trop J Pharm Res 2023; 22(2):271-276 doi: 10.4314/tjpr.v22i2.7

© 2023 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: To examine the association of propofol (PRO) with related key genes that may serve as potential biomarkers for alleviation of PRO-induced toxicity in neural stem cells (NSCs).

Methods: Differentially expressed genes (DEGs) were screened based on GEO database, using the analysis platform of Metaboanalyst, GEO2R, DAVID and Ehbio. NSCs were purchased and treated with 3 μM of propofol (PRO). NR4A1 was transfected into NSCs, and the NR4A1 expression, apoptosis-related protein and AMPK pathway-related protein were determined by quantitative reverse transcription-polymerase chain reaction (qRT-PCR) and western blotting. Cell viability and apoptosis were evaluated by methylthiazolyldiphenyl-tetrazolium bromid (MTT) assay and flow cytometry.

Results: A total of 278 DEGs were analyzed on GSE106799 microarray, and finally screened for differentially expressed down-regulated gene, NR4A1, which is a hubgene. NR4A1 expression decreased in PRO-induced NSCs. Furthermore, NR4A1 attenuated the PRO-induced decrease in the viability of NSCs and the increase in apoptosis. Moreover, NR4A1 increased p-AMPK/AMPK level.

Conclusion: NR4A1 attenuates the toxicity in NSCs induced by PRO by regulating AMPK pathways, and thus provides a theoretical basis for the treatment of nerve damage caused by anesthetics.

Keywords: NR4A1, Eural stem cells, AMPK, Propofol, Hubgene