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D-galactose protects the intestine from ionizing radiation-induced injury by altering the gut microbiome

This article aims to investigate the protection of the intestine from ionizing radiation-induced injury by using D-galactose (D-gal) to alter the gut microbiome. In addition, this observation opens up further lines of research to further increase therapeutic potentials. Male C57BL/6 mice were expose...

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Detalles Bibliográficos
Autores principales: Zhu, Tong, Wang, Zhouxuan, He, Junbo, Zhang, Xueying, Zhu, Changchun, Zhang, Shuqin, Li, Yuan, Fan, Saijun
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Oxford University Press 2022
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9726703/
https://www.ncbi.nlm.nih.gov/pubmed/36253108
http://dx.doi.org/10.1093/jrr/rrac059
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author Zhu, Tong
Wang, Zhouxuan
He, Junbo
Zhang, Xueying
Zhu, Changchun
Zhang, Shuqin
Li, Yuan
Fan, Saijun
author_facet Zhu, Tong
Wang, Zhouxuan
He, Junbo
Zhang, Xueying
Zhu, Changchun
Zhang, Shuqin
Li, Yuan
Fan, Saijun
author_sort Zhu, Tong
collection PubMed
description This article aims to investigate the protection of the intestine from ionizing radiation-induced injury by using D-galactose (D-gal) to alter the gut microbiome. In addition, this observation opens up further lines of research to further increase therapeutic potentials. Male C57BL/6 mice were exposed to 7.5 Gy of total body irradiation (TBI) or 13 Gy of total abdominal irradiation (TAI) in this study. After adjustment, D-gal was intraperitoneally injected into mice at a dose of 750 mg/kg/day. Survival rates, body weights, histological experiments and the level of the inflammatory factor IL-1β were observed after TBI to investigate radiation injury in mice. Feces were collected from mice for 16S high-throughput sequencing after TAI. Furthermore, fecal microorganism transplantation (FMT) was performed to confirm the effect of D-gal on radiation injury recovery. Intraperitoneally administered D-gal significantly increased the survival of irradiated mice by altering the gut microbiota structure. Furthermore, the fecal microbiota transplanted from D-gal-treated mice protected against radiation injury and improved the survival rate of recipient mice. Taken together, D-gal accelerates gut recovery following radiation injury by promoting the growth of specific microorganisms, especially those in the class Erysipelotrichia. The study discovered that D-gal-induced changes in the microbiota protect against radiation-induced intestinal injury. Erysipelotrichia and its metabolites are a promising therapeutic option for post-radiation intestinal regeneration.
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spelling pubmed-97267032022-12-08 D-galactose protects the intestine from ionizing radiation-induced injury by altering the gut microbiome Zhu, Tong Wang, Zhouxuan He, Junbo Zhang, Xueying Zhu, Changchun Zhang, Shuqin Li, Yuan Fan, Saijun J Radiat Res Regular paper This article aims to investigate the protection of the intestine from ionizing radiation-induced injury by using D-galactose (D-gal) to alter the gut microbiome. In addition, this observation opens up further lines of research to further increase therapeutic potentials. Male C57BL/6 mice were exposed to 7.5 Gy of total body irradiation (TBI) or 13 Gy of total abdominal irradiation (TAI) in this study. After adjustment, D-gal was intraperitoneally injected into mice at a dose of 750 mg/kg/day. Survival rates, body weights, histological experiments and the level of the inflammatory factor IL-1β were observed after TBI to investigate radiation injury in mice. Feces were collected from mice for 16S high-throughput sequencing after TAI. Furthermore, fecal microorganism transplantation (FMT) was performed to confirm the effect of D-gal on radiation injury recovery. Intraperitoneally administered D-gal significantly increased the survival of irradiated mice by altering the gut microbiota structure. Furthermore, the fecal microbiota transplanted from D-gal-treated mice protected against radiation injury and improved the survival rate of recipient mice. Taken together, D-gal accelerates gut recovery following radiation injury by promoting the growth of specific microorganisms, especially those in the class Erysipelotrichia. The study discovered that D-gal-induced changes in the microbiota protect against radiation-induced intestinal injury. Erysipelotrichia and its metabolites are a promising therapeutic option for post-radiation intestinal regeneration. Oxford University Press 2022-10-17 /pmc/articles/PMC9726703/ /pubmed/36253108 http://dx.doi.org/10.1093/jrr/rrac059 Text en © The Author(s) 2022. Published by Oxford University Press on behalf of The Japanese Radiation Research Society and Japanese Society for Radiation Oncology. https://creativecommons.org/licenses/by-nc/4.0/This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (https://creativecommons.org/licenses/by-nc/4.0/), which permits non-commercial re-use, distribution, and reproduction in any medium, provided the original work is properly cited. For commercial re-use, please contact journals.permissions@oup.com
spellingShingle Regular paper
Zhu, Tong
Wang, Zhouxuan
He, Junbo
Zhang, Xueying
Zhu, Changchun
Zhang, Shuqin
Li, Yuan
Fan, Saijun
D-galactose protects the intestine from ionizing radiation-induced injury by altering the gut microbiome
title D-galactose protects the intestine from ionizing radiation-induced injury by altering the gut microbiome
title_full D-galactose protects the intestine from ionizing radiation-induced injury by altering the gut microbiome
title_fullStr D-galactose protects the intestine from ionizing radiation-induced injury by altering the gut microbiome
title_full_unstemmed D-galactose protects the intestine from ionizing radiation-induced injury by altering the gut microbiome
title_short D-galactose protects the intestine from ionizing radiation-induced injury by altering the gut microbiome
title_sort d-galactose protects the intestine from ionizing radiation-induced injury by altering the gut microbiome
topic Regular paper
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9726703/
https://www.ncbi.nlm.nih.gov/pubmed/36253108
http://dx.doi.org/10.1093/jrr/rrac059
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