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Intraperitoneal hypertension, a novel risk factor for sepsis-associated encephalopathy in sepsis mice
Sepsis associated encephalopathy (SAE), appears often indicates the deterioration of the sepsis disease and which have high risk of death. Although several mechanism and hypotheses have been proposed and studied, there is no breakthrough in the treatment of SAE. We performed a systematic research to...
Autores principales: | , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Nature Publishing Group UK
2018
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5970176/ https://www.ncbi.nlm.nih.gov/pubmed/29802336 http://dx.doi.org/10.1038/s41598-018-26500-7 |
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author | He, Yu-jing Xu, Hao Fu, Yao-jie Lin, Ji-yan Zhang, Min-wei |
author_facet | He, Yu-jing Xu, Hao Fu, Yao-jie Lin, Ji-yan Zhang, Min-wei |
author_sort | He, Yu-jing |
collection | PubMed |
description | Sepsis associated encephalopathy (SAE), appears often indicates the deterioration of the sepsis disease and which have high risk of death. Although several mechanism and hypotheses have been proposed and studied, there is no breakthrough in the treatment of SAE. We performed a systematic research to evaluate the effect of intraperitoneal pressure on SAE. A mice model of sepsis was established by intraperitoneal injection of endotoxin. A total of 48 female BALB/c mouse (30 days old) were randomly divided into a control group (n = 12) and an injection of endotoxin referred to bacterial lipopolysaccharide (LPS) group (n = 12). Intraperitoneal hypertension (IAH) referred to IAH group (n = 12), and LPS + IAH group (n = 12). Following sepsis induction, diagnosis, the brains were analyzed for both function and ultrastructural morphology.We determined that IAH exacerbated sepsis induces sepsis-associated encephalopathy when examining low score of neurological function and more delta wave in EEG, increased neuronal edema in LPS + IAH group, as well as an escalation of Bax and Cleaved-caspase-3, Cleaved-parp, and reduction of Bcl-2 and Mfsd2a in LPS + IAH group. Therefore, IAH can exacerbate and increase incident rate of sepsis-related encephalopathy in sepsis mice by promoting neuronal apoptosis and destruction of the blood-brain barrier. |
format | Online Article Text |
id | pubmed-5970176 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2018 |
publisher | Nature Publishing Group UK |
record_format | MEDLINE/PubMed |
spelling | pubmed-59701762018-05-30 Intraperitoneal hypertension, a novel risk factor for sepsis-associated encephalopathy in sepsis mice He, Yu-jing Xu, Hao Fu, Yao-jie Lin, Ji-yan Zhang, Min-wei Sci Rep Article Sepsis associated encephalopathy (SAE), appears often indicates the deterioration of the sepsis disease and which have high risk of death. Although several mechanism and hypotheses have been proposed and studied, there is no breakthrough in the treatment of SAE. We performed a systematic research to evaluate the effect of intraperitoneal pressure on SAE. A mice model of sepsis was established by intraperitoneal injection of endotoxin. A total of 48 female BALB/c mouse (30 days old) were randomly divided into a control group (n = 12) and an injection of endotoxin referred to bacterial lipopolysaccharide (LPS) group (n = 12). Intraperitoneal hypertension (IAH) referred to IAH group (n = 12), and LPS + IAH group (n = 12). Following sepsis induction, diagnosis, the brains were analyzed for both function and ultrastructural morphology.We determined that IAH exacerbated sepsis induces sepsis-associated encephalopathy when examining low score of neurological function and more delta wave in EEG, increased neuronal edema in LPS + IAH group, as well as an escalation of Bax and Cleaved-caspase-3, Cleaved-parp, and reduction of Bcl-2 and Mfsd2a in LPS + IAH group. Therefore, IAH can exacerbate and increase incident rate of sepsis-related encephalopathy in sepsis mice by promoting neuronal apoptosis and destruction of the blood-brain barrier. Nature Publishing Group UK 2018-05-25 /pmc/articles/PMC5970176/ /pubmed/29802336 http://dx.doi.org/10.1038/s41598-018-26500-7 Text en © The Author(s) 2018 Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/. |
spellingShingle | Article He, Yu-jing Xu, Hao Fu, Yao-jie Lin, Ji-yan Zhang, Min-wei Intraperitoneal hypertension, a novel risk factor for sepsis-associated encephalopathy in sepsis mice |
title | Intraperitoneal hypertension, a novel risk factor for sepsis-associated encephalopathy in sepsis mice |
title_full | Intraperitoneal hypertension, a novel risk factor for sepsis-associated encephalopathy in sepsis mice |
title_fullStr | Intraperitoneal hypertension, a novel risk factor for sepsis-associated encephalopathy in sepsis mice |
title_full_unstemmed | Intraperitoneal hypertension, a novel risk factor for sepsis-associated encephalopathy in sepsis mice |
title_short | Intraperitoneal hypertension, a novel risk factor for sepsis-associated encephalopathy in sepsis mice |
title_sort | intraperitoneal hypertension, a novel risk factor for sepsis-associated encephalopathy in sepsis mice |
topic | Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5970176/ https://www.ncbi.nlm.nih.gov/pubmed/29802336 http://dx.doi.org/10.1038/s41598-018-26500-7 |
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