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Glucose Starvation-Caused Oxidative Stress Induces Inflammation and Autophagy in Human Gingival Fibroblasts
Gingival tissue experiences an environment of nutrient shortage, such as low glucose conditions, after periodontal surgery. Our previous studies found that this low glucose condition inhibits normal gingival cell functions. However, the mechanism by which this glucose-deficient environment causes ce...
Autores principales: | , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
MDPI
2022
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9598069/ https://www.ncbi.nlm.nih.gov/pubmed/36290630 http://dx.doi.org/10.3390/antiox11101907 |
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author | Li, Runbo Kato, Hirohito Taguchi, Yoichiro Deng, Xin Minagawa, Emika Nakata, Takaya Umeda, Makoto |
author_facet | Li, Runbo Kato, Hirohito Taguchi, Yoichiro Deng, Xin Minagawa, Emika Nakata, Takaya Umeda, Makoto |
author_sort | Li, Runbo |
collection | PubMed |
description | Gingival tissue experiences an environment of nutrient shortage, such as low glucose conditions, after periodontal surgery. Our previous studies found that this low glucose condition inhibits normal gingival cell functions. However, the mechanism by which this glucose-deficient environment causes cellular damage to human gingival fibroblasts (HGnFs) remains unclear. This study aimed to investigate the biological effects of ROS induction on HGnFs under low glucose conditions. ROS levels and cellular anti-ROS ability of HGnFs under different glucose concentrations were evaluated by measuring ROS formation and the expression of superoxide dismutase and heme oxygenase 1. Changes in cellular viability were investigated using 5-bromo-2′-deoxyuridine assay and cell survival detection, and the cellular damage was evaluated by the expression of inflammatory cytokines and changes in the expression of autophagy-related protein. ROS formation was then blocked using N-acetyl-L-cysteine (NAC), and the effects of ROS on HGnFs under low glucose conditions were investigated. Low glucose conditions induced ROS accumulation, reduced cellular activity, and induced inflammation and autophagy. After NAC application, the anti-ROS capacity increased, cellular activity improved, and inflammation and autophagy were controlled. This can be effectively controlled by the application of antioxidants such as NAC. |
format | Online Article Text |
id | pubmed-9598069 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2022 |
publisher | MDPI |
record_format | MEDLINE/PubMed |
spelling | pubmed-95980692022-10-27 Glucose Starvation-Caused Oxidative Stress Induces Inflammation and Autophagy in Human Gingival Fibroblasts Li, Runbo Kato, Hirohito Taguchi, Yoichiro Deng, Xin Minagawa, Emika Nakata, Takaya Umeda, Makoto Antioxidants (Basel) Article Gingival tissue experiences an environment of nutrient shortage, such as low glucose conditions, after periodontal surgery. Our previous studies found that this low glucose condition inhibits normal gingival cell functions. However, the mechanism by which this glucose-deficient environment causes cellular damage to human gingival fibroblasts (HGnFs) remains unclear. This study aimed to investigate the biological effects of ROS induction on HGnFs under low glucose conditions. ROS levels and cellular anti-ROS ability of HGnFs under different glucose concentrations were evaluated by measuring ROS formation and the expression of superoxide dismutase and heme oxygenase 1. Changes in cellular viability were investigated using 5-bromo-2′-deoxyuridine assay and cell survival detection, and the cellular damage was evaluated by the expression of inflammatory cytokines and changes in the expression of autophagy-related protein. ROS formation was then blocked using N-acetyl-L-cysteine (NAC), and the effects of ROS on HGnFs under low glucose conditions were investigated. Low glucose conditions induced ROS accumulation, reduced cellular activity, and induced inflammation and autophagy. After NAC application, the anti-ROS capacity increased, cellular activity improved, and inflammation and autophagy were controlled. This can be effectively controlled by the application of antioxidants such as NAC. MDPI 2022-09-26 /pmc/articles/PMC9598069/ /pubmed/36290630 http://dx.doi.org/10.3390/antiox11101907 Text en © 2022 by the authors. https://creativecommons.org/licenses/by/4.0/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/). |
spellingShingle | Article Li, Runbo Kato, Hirohito Taguchi, Yoichiro Deng, Xin Minagawa, Emika Nakata, Takaya Umeda, Makoto Glucose Starvation-Caused Oxidative Stress Induces Inflammation and Autophagy in Human Gingival Fibroblasts |
title | Glucose Starvation-Caused Oxidative Stress Induces Inflammation and Autophagy in Human Gingival Fibroblasts |
title_full | Glucose Starvation-Caused Oxidative Stress Induces Inflammation and Autophagy in Human Gingival Fibroblasts |
title_fullStr | Glucose Starvation-Caused Oxidative Stress Induces Inflammation and Autophagy in Human Gingival Fibroblasts |
title_full_unstemmed | Glucose Starvation-Caused Oxidative Stress Induces Inflammation and Autophagy in Human Gingival Fibroblasts |
title_short | Glucose Starvation-Caused Oxidative Stress Induces Inflammation and Autophagy in Human Gingival Fibroblasts |
title_sort | glucose starvation-caused oxidative stress induces inflammation and autophagy in human gingival fibroblasts |
topic | Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9598069/ https://www.ncbi.nlm.nih.gov/pubmed/36290630 http://dx.doi.org/10.3390/antiox11101907 |
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