Cargando…

Glutamine relieves oxidative stress through PI3K/Akt signaling pathway in DSS-induced ulcerative colitis mice

OBJECTIVE(S): Ulcerative colitis (UC) is a kind of complex immune disease, and a major cause of destruction of intestinal barrier and oxidative stress in this field. In this paper, glutamine (Gln) was believed to offer protection against oxidative stress injury in colitis mice. MATERIALS AND METHODS...

Descripción completa

Detalles Bibliográficos
Autores principales: Yan, Shuguang, Hui, Yi, Li, Jingtao, Xu, Xiaofan, Li, Qian, Wei, Hailiang
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Mashhad University of Medical Sciences 2020
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7491493/
https://www.ncbi.nlm.nih.gov/pubmed/32963733
http://dx.doi.org/10.22038/ijbms.2020.39815.9436
_version_ 1783582229598830592
author Yan, Shuguang
Hui, Yi
Li, Jingtao
Xu, Xiaofan
Li, Qian
Wei, Hailiang
author_facet Yan, Shuguang
Hui, Yi
Li, Jingtao
Xu, Xiaofan
Li, Qian
Wei, Hailiang
author_sort Yan, Shuguang
collection PubMed
description OBJECTIVE(S): Ulcerative colitis (UC) is a kind of complex immune disease, and a major cause of destruction of intestinal barrier and oxidative stress in this field. In this paper, glutamine (Gln) was believed to offer protection against oxidative stress injury in colitis mice. MATERIALS AND METHODS: Thirty mice were randomly assigned into control, model, LY294002 (PI3K/Akt inhibitor), Gln, Gln+LY294002 and 5-Aminosalicylic acid (5-ASA) groups. The mice in the experimental group drank 4% dextran sulfate sodium salt (DSS) for 7 consecutive days. The protective effect of Gln on oxidative stress was quantified by keeping colitis mice, involving Phosphatidylinositol-3-kinase (PI3K)/Protein kinase B (Akt)/mammalian target of Rapamycin (mTOR) signaling pathway, with different medications or distilled water through intragastric administration for 10 consecutive days. RESULTS: In vivo administration of Gln, LY294002 or 5-ASA was found to ameliorate the symptoms of colitis in mice, such as reduced growth, loose stools and stool bleeding; protected DSS-induced colitis mice from goblet cell loss, lymphocytosis, mucosal erosion, loss of crypts, and neutrophil infiltration; improved the activity of superoxide dismutase (SOD) and glutathione peroxidase (GSH-XP); decreased the content of malondialdehyde (MDA); and inhibited the activation of PI3K/Akt signaling pathway. CONCLUSION: Administration of Gln to the DSS-induced colitis mice led to a clearly reduction in oxidative stress-induced injury. The Gln is confirmed as inhibiting the PI3K/Akt signaling pathway activity.
format Online
Article
Text
id pubmed-7491493
institution National Center for Biotechnology Information
language English
publishDate 2020
publisher Mashhad University of Medical Sciences
record_format MEDLINE/PubMed
spelling pubmed-74914932020-09-21 Glutamine relieves oxidative stress through PI3K/Akt signaling pathway in DSS-induced ulcerative colitis mice Yan, Shuguang Hui, Yi Li, Jingtao Xu, Xiaofan Li, Qian Wei, Hailiang Iran J Basic Med Sci Original Article OBJECTIVE(S): Ulcerative colitis (UC) is a kind of complex immune disease, and a major cause of destruction of intestinal barrier and oxidative stress in this field. In this paper, glutamine (Gln) was believed to offer protection against oxidative stress injury in colitis mice. MATERIALS AND METHODS: Thirty mice were randomly assigned into control, model, LY294002 (PI3K/Akt inhibitor), Gln, Gln+LY294002 and 5-Aminosalicylic acid (5-ASA) groups. The mice in the experimental group drank 4% dextran sulfate sodium salt (DSS) for 7 consecutive days. The protective effect of Gln on oxidative stress was quantified by keeping colitis mice, involving Phosphatidylinositol-3-kinase (PI3K)/Protein kinase B (Akt)/mammalian target of Rapamycin (mTOR) signaling pathway, with different medications or distilled water through intragastric administration for 10 consecutive days. RESULTS: In vivo administration of Gln, LY294002 or 5-ASA was found to ameliorate the symptoms of colitis in mice, such as reduced growth, loose stools and stool bleeding; protected DSS-induced colitis mice from goblet cell loss, lymphocytosis, mucosal erosion, loss of crypts, and neutrophil infiltration; improved the activity of superoxide dismutase (SOD) and glutathione peroxidase (GSH-XP); decreased the content of malondialdehyde (MDA); and inhibited the activation of PI3K/Akt signaling pathway. CONCLUSION: Administration of Gln to the DSS-induced colitis mice led to a clearly reduction in oxidative stress-induced injury. The Gln is confirmed as inhibiting the PI3K/Akt signaling pathway activity. Mashhad University of Medical Sciences 2020-09 /pmc/articles/PMC7491493/ /pubmed/32963733 http://dx.doi.org/10.22038/ijbms.2020.39815.9436 Text en This is an Open Access article distributed under the terms of the Creative Commons Attribution License, (http://creativecommons.org/licenses/by/3.0/) which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Original Article
Yan, Shuguang
Hui, Yi
Li, Jingtao
Xu, Xiaofan
Li, Qian
Wei, Hailiang
Glutamine relieves oxidative stress through PI3K/Akt signaling pathway in DSS-induced ulcerative colitis mice
title Glutamine relieves oxidative stress through PI3K/Akt signaling pathway in DSS-induced ulcerative colitis mice
title_full Glutamine relieves oxidative stress through PI3K/Akt signaling pathway in DSS-induced ulcerative colitis mice
title_fullStr Glutamine relieves oxidative stress through PI3K/Akt signaling pathway in DSS-induced ulcerative colitis mice
title_full_unstemmed Glutamine relieves oxidative stress through PI3K/Akt signaling pathway in DSS-induced ulcerative colitis mice
title_short Glutamine relieves oxidative stress through PI3K/Akt signaling pathway in DSS-induced ulcerative colitis mice
title_sort glutamine relieves oxidative stress through pi3k/akt signaling pathway in dss-induced ulcerative colitis mice
topic Original Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7491493/
https://www.ncbi.nlm.nih.gov/pubmed/32963733
http://dx.doi.org/10.22038/ijbms.2020.39815.9436
work_keys_str_mv AT yanshuguang glutaminerelievesoxidativestressthroughpi3kaktsignalingpathwayindssinducedulcerativecolitismice
AT huiyi glutaminerelievesoxidativestressthroughpi3kaktsignalingpathwayindssinducedulcerativecolitismice
AT lijingtao glutaminerelievesoxidativestressthroughpi3kaktsignalingpathwayindssinducedulcerativecolitismice
AT xuxiaofan glutaminerelievesoxidativestressthroughpi3kaktsignalingpathwayindssinducedulcerativecolitismice
AT liqian glutaminerelievesoxidativestressthroughpi3kaktsignalingpathwayindssinducedulcerativecolitismice
AT weihailiang glutaminerelievesoxidativestressthroughpi3kaktsignalingpathwayindssinducedulcerativecolitismice