Cargando…

Hyperbaric oxygen protects HT22 cells and PC12 cells from damage caused by oxygen-glucose deprivation/reperfusion via the inhibition of Nrf2/System Xc-/GPX4 axis-mediated ferroptosis

This study was to investigate the protective effect of hyperbaric oxygen (HBO) on HT22 and PC12 cell damage caused by oxygen-glucose deprivation/reperfusion-induced ferroptosis. A 2-h oxygen-glucose deprivation and 24-h reperfusion model on HT22 and PC12 cells was used to simulate cerebral ischemia-...

Descripción completa

Detalles Bibliográficos
Autores principales: Chen, Chunxia, Chen, Wan, Zhou, Xing, Li, Yaoxuan, Pan, Xiaorong, Chen, Xiaoyu
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Public Library of Science 2022
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9648730/
https://www.ncbi.nlm.nih.gov/pubmed/36355759
http://dx.doi.org/10.1371/journal.pone.0276083
_version_ 1784827640206589952
author Chen, Chunxia
Chen, Wan
Zhou, Xing
Li, Yaoxuan
Pan, Xiaorong
Chen, Xiaoyu
author_facet Chen, Chunxia
Chen, Wan
Zhou, Xing
Li, Yaoxuan
Pan, Xiaorong
Chen, Xiaoyu
author_sort Chen, Chunxia
collection PubMed
description This study was to investigate the protective effect of hyperbaric oxygen (HBO) on HT22 and PC12 cell damage caused by oxygen-glucose deprivation/reperfusion-induced ferroptosis. A 2-h oxygen-glucose deprivation and 24-h reperfusion model on HT22 and PC12 cells was used to simulate cerebral ischemia-reperfusion injury. Cell viabilities were detected by Cell Counting Kit-8 (CCK-8) method. The levels of reactive oxygen species (ROS) and lipid reactive oxygen species (Lipid ROS) were detected by fluorescent probes Dihydroethidium (DHE) and C11 BODIPY 581/591. Iron Colorimetric Assay Kit, malondialdehyde (MDA) and glutathione (GSH) activity assay kits were used to detect intracellular iron ion, MDA and GSHcontent. Cell ferroptosis-related ultrastructures were visualized using transmission electron microscopy (TEM). Furthermore, PCR and Western blot analyses were used to detect the expressions of ferroptosis-related genes and proteins. After receiving oxygen-glucose deprivation/reperfusion, the viabilities of HT22 and PC12 cells were significantly decreased; ROS, Lipid ROS, iron ions and MDA accumulation occurred in the cells; GSH contents decreased; TEM showed that cells were ruptured and blebbed, mitochondria atrophied and became smaller, mitochondrial ridges were reduced or even disappeared, and apoptotic bodies appeared. And the expressions of Nrf2, SLC7A11 and GPX4 genes were reduced; the expressions of p-Nrf2/Nrf2, xCT and GPX4 proteins were reduced. Notably, these parameters were significantly reversed by HBO, indicating that HBO can protect HT22 cells and PC12 cells from damage caused by oxygen-glucosedeprivation/reperfusion via the inhibition of Nrf2/System Xc-/GPX4 axis-mediated ferroptosis.
format Online
Article
Text
id pubmed-9648730
institution National Center for Biotechnology Information
language English
publishDate 2022
publisher Public Library of Science
record_format MEDLINE/PubMed
spelling pubmed-96487302022-11-15 Hyperbaric oxygen protects HT22 cells and PC12 cells from damage caused by oxygen-glucose deprivation/reperfusion via the inhibition of Nrf2/System Xc-/GPX4 axis-mediated ferroptosis Chen, Chunxia Chen, Wan Zhou, Xing Li, Yaoxuan Pan, Xiaorong Chen, Xiaoyu PLoS One Research Article This study was to investigate the protective effect of hyperbaric oxygen (HBO) on HT22 and PC12 cell damage caused by oxygen-glucose deprivation/reperfusion-induced ferroptosis. A 2-h oxygen-glucose deprivation and 24-h reperfusion model on HT22 and PC12 cells was used to simulate cerebral ischemia-reperfusion injury. Cell viabilities were detected by Cell Counting Kit-8 (CCK-8) method. The levels of reactive oxygen species (ROS) and lipid reactive oxygen species (Lipid ROS) were detected by fluorescent probes Dihydroethidium (DHE) and C11 BODIPY 581/591. Iron Colorimetric Assay Kit, malondialdehyde (MDA) and glutathione (GSH) activity assay kits were used to detect intracellular iron ion, MDA and GSHcontent. Cell ferroptosis-related ultrastructures were visualized using transmission electron microscopy (TEM). Furthermore, PCR and Western blot analyses were used to detect the expressions of ferroptosis-related genes and proteins. After receiving oxygen-glucose deprivation/reperfusion, the viabilities of HT22 and PC12 cells were significantly decreased; ROS, Lipid ROS, iron ions and MDA accumulation occurred in the cells; GSH contents decreased; TEM showed that cells were ruptured and blebbed, mitochondria atrophied and became smaller, mitochondrial ridges were reduced or even disappeared, and apoptotic bodies appeared. And the expressions of Nrf2, SLC7A11 and GPX4 genes were reduced; the expressions of p-Nrf2/Nrf2, xCT and GPX4 proteins were reduced. Notably, these parameters were significantly reversed by HBO, indicating that HBO can protect HT22 cells and PC12 cells from damage caused by oxygen-glucosedeprivation/reperfusion via the inhibition of Nrf2/System Xc-/GPX4 axis-mediated ferroptosis. Public Library of Science 2022-11-10 /pmc/articles/PMC9648730/ /pubmed/36355759 http://dx.doi.org/10.1371/journal.pone.0276083 Text en © 2022 Chen et al https://creativecommons.org/licenses/by/4.0/This is an open access article distributed under the terms of the Creative Commons Attribution License (https://creativecommons.org/licenses/by/4.0/) , which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
spellingShingle Research Article
Chen, Chunxia
Chen, Wan
Zhou, Xing
Li, Yaoxuan
Pan, Xiaorong
Chen, Xiaoyu
Hyperbaric oxygen protects HT22 cells and PC12 cells from damage caused by oxygen-glucose deprivation/reperfusion via the inhibition of Nrf2/System Xc-/GPX4 axis-mediated ferroptosis
title Hyperbaric oxygen protects HT22 cells and PC12 cells from damage caused by oxygen-glucose deprivation/reperfusion via the inhibition of Nrf2/System Xc-/GPX4 axis-mediated ferroptosis
title_full Hyperbaric oxygen protects HT22 cells and PC12 cells from damage caused by oxygen-glucose deprivation/reperfusion via the inhibition of Nrf2/System Xc-/GPX4 axis-mediated ferroptosis
title_fullStr Hyperbaric oxygen protects HT22 cells and PC12 cells from damage caused by oxygen-glucose deprivation/reperfusion via the inhibition of Nrf2/System Xc-/GPX4 axis-mediated ferroptosis
title_full_unstemmed Hyperbaric oxygen protects HT22 cells and PC12 cells from damage caused by oxygen-glucose deprivation/reperfusion via the inhibition of Nrf2/System Xc-/GPX4 axis-mediated ferroptosis
title_short Hyperbaric oxygen protects HT22 cells and PC12 cells from damage caused by oxygen-glucose deprivation/reperfusion via the inhibition of Nrf2/System Xc-/GPX4 axis-mediated ferroptosis
title_sort hyperbaric oxygen protects ht22 cells and pc12 cells from damage caused by oxygen-glucose deprivation/reperfusion via the inhibition of nrf2/system xc-/gpx4 axis-mediated ferroptosis
topic Research Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9648730/
https://www.ncbi.nlm.nih.gov/pubmed/36355759
http://dx.doi.org/10.1371/journal.pone.0276083
work_keys_str_mv AT chenchunxia hyperbaricoxygenprotectsht22cellsandpc12cellsfromdamagecausedbyoxygenglucosedeprivationreperfusionviatheinhibitionofnrf2systemxcgpx4axismediatedferroptosis
AT chenwan hyperbaricoxygenprotectsht22cellsandpc12cellsfromdamagecausedbyoxygenglucosedeprivationreperfusionviatheinhibitionofnrf2systemxcgpx4axismediatedferroptosis
AT zhouxing hyperbaricoxygenprotectsht22cellsandpc12cellsfromdamagecausedbyoxygenglucosedeprivationreperfusionviatheinhibitionofnrf2systemxcgpx4axismediatedferroptosis
AT liyaoxuan hyperbaricoxygenprotectsht22cellsandpc12cellsfromdamagecausedbyoxygenglucosedeprivationreperfusionviatheinhibitionofnrf2systemxcgpx4axismediatedferroptosis
AT panxiaorong hyperbaricoxygenprotectsht22cellsandpc12cellsfromdamagecausedbyoxygenglucosedeprivationreperfusionviatheinhibitionofnrf2systemxcgpx4axismediatedferroptosis
AT chenxiaoyu hyperbaricoxygenprotectsht22cellsandpc12cellsfromdamagecausedbyoxygenglucosedeprivationreperfusionviatheinhibitionofnrf2systemxcgpx4axismediatedferroptosis