Issue 60, 2019

Attenuated glutamate induced ROS production by antioxidative compounds in neural cell lines

Abstract

Glutamate is an excitatory neurotransmitter involved in neural function. Excess accumulation of intercellular glutamate leads to increasing concentration of reactive oxygen species (ROS) and reactive nitrogen species (RNS) in neuronal cells. In this study, we investigated the antioxidant activity of several typical superior compounds among four neuronal cells, and determined the scavenging activity of free radicals. The in vivo assay was also carried out to compare the protective effect of glutamate-induced cell damage. Hierarchical clustering analysis was used to identify the common properties. Glutamate induced neurotoxicity and ROS production, suggesting glutamate cytotoxicity was related to oxidative stress and widely exists in different cell lines. Those screening compounds exhibited strong antioxidant ability, but low cytotoxicity to neuronal cells, acting as agents against neurodegenerative diseases. Finally, a hierarchical clustering analysis assay indicated that hyperoside and rutin hydrate are the most effective compounds for attenuating intercellular ROS levels. The results suggested the activity more or less relies on structure, rather than residues. These data generate new supporting ideas to remove intracellular ROS and the identified compounds serve as potential therapeutic agents in multiple neurological diseases.

Graphical abstract: Attenuated glutamate induced ROS production by antioxidative compounds in neural cell lines

Article information

Article type
Paper
Submitted
22 May 2019
Accepted
21 Oct 2019
First published
28 Oct 2019
This article is Open Access
Creative Commons BY license

RSC Adv., 2019,9, 34735-34743

Attenuated glutamate induced ROS production by antioxidative compounds in neural cell lines

H. Xin, Y. Cui, Z. An, Q. Yang, X. Zou and N. Yu, RSC Adv., 2019, 9, 34735 DOI: 10.1039/C9RA03848E

This article is licensed under a Creative Commons Attribution 3.0 Unported Licence. You can use material from this article in other publications without requesting further permissions from the RSC, provided that the correct acknowledgement is given.

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