Figure - PMC

Skip to main content

An official website of the United States government

Here's how you know

Here's how you know

Official websites use .gov
A .gov website belongs to an official government organization in the United States.

Secure .gov websites use HTTPS
A lock ( ) or https:// means you've safely connected to the .gov website. Share sensitive information only on official, secure websites.

View full-text article in PMC

. 2022 Jan 17;11(1):170. doi: 10.3390/antiox11010170

Search in PMC
Search in PubMed
View in NLM Catalog
Add to search

© 2022 by the authors.

Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/).

PMC Copyright notice

Neuroprotective astrocyte by antioxidants in concert with microglia. Astrocytes are known to play neurotoxic roles in neurodegenerative diseases. Microglia can induce neurotoxic astrocytes through Toll-like receptor (TLR) 4 activation. Reactive oxygen species (ROSs) and nitric oxide (NO) act as neurotoxic molecules that can cause neuronal injury. We focused on the neuroprotective roles of astrocytes through their high glycolysis activity and the pentose–phosphate pathway (PPP) against oxidative stress. Alpha-synuclein and lipopolysaccharide (LPS), a natural TLR4 ligand, induce ROS and NO production in microglia. We found that NO released from microglia activated astroglial PPP flux through the Kelch-like enoyl-CoA hydratase-associated protein 1 (Keap1)/nuclear factor erythroid 2 p45 subunit-related factor 2 (Nrf2) system. Namely, the NO-induced nitrosylation of Keap1 residues released Nrf2 from Keap1, allowing Nrf2 to act as a transcription factor in an in vitro model of cultured rodent microglia and astroglia.