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Postconditioning improvement effects of ulinastatin on brain injury following cardiopulmonary resuscitation

The aim of the present study was to determine the effects of ulinastatin (UTI) on brain injury in rats subjected to cardiopulmonary resuscitation (CPR) following asphyxial cardiac arrest (CA) and identify the underlying mechanisms. In total, 100 healthy male Wistar rats were randomly divided into co...

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Autores principales: SUI, BO, LI, YONGWANG, MA, LI
Formato: Online Artículo Texto
Lenguaje:English
Publicado: D.A. Spandidos 2014
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4151659/
https://www.ncbi.nlm.nih.gov/pubmed/25187844
http://dx.doi.org/10.3892/etm.2014.1876
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author SUI, BO
LI, YONGWANG
MA, LI
author_facet SUI, BO
LI, YONGWANG
MA, LI
author_sort SUI, BO
collection PubMed
description The aim of the present study was to determine the effects of ulinastatin (UTI) on brain injury in rats subjected to cardiopulmonary resuscitation (CPR) following asphyxial cardiac arrest (CA) and identify the underlying mechanisms. In total, 100 healthy male Wistar rats were randomly divided into control and treatment groups (n=50). After 4 min of asphyxial CA, all the rats were immediately subjected to CPR. The treatment group animals were administered 15 mg/kg UTI at the onset of resuscitation. The mortality rate in the two groups was recorded at 24 h post-resuscitation. In addition, neurological function was evaluated at 24, 48 and 72 h post-resuscitation using a neurological deficit scale (NDS). Furthermore, the effects of UTI on the Toll-like receptor 4 (TLR4) signaling pathway in brain tissues were determined by assessing TLR4 mRNA expression, nuclear factor (NF)-κB activity and tumor necrosis factor (TNF)-α and interleukin (IL)-6 levels at 1, 3, 6, 12, 24, 48 and 72 h post-resuscitation. After 24 h, the mortality rate significantly decreased in the treatment group when compared with the control animals (10 vs. 30%; P<0.05). Additionally, an overt improvement was observed in the NDS score following UTI treatment when compared with the control (P<0.01). Finally, statistically significant decreases in the levels of TLR4 mRNA expression, NF-κB activity and TNF-α and IL-6 were observed in the treatment group at each time point (P<0.01). Therefore, UTI treatment at the onset of CPR significantly inhibits the TLR4 signaling pathway, thereby alleviating the inflammatory responses following resuscitation and improving neurological function.
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spelling pubmed-41516592014-09-03 Postconditioning improvement effects of ulinastatin on brain injury following cardiopulmonary resuscitation SUI, BO LI, YONGWANG MA, LI Exp Ther Med Articles The aim of the present study was to determine the effects of ulinastatin (UTI) on brain injury in rats subjected to cardiopulmonary resuscitation (CPR) following asphyxial cardiac arrest (CA) and identify the underlying mechanisms. In total, 100 healthy male Wistar rats were randomly divided into control and treatment groups (n=50). After 4 min of asphyxial CA, all the rats were immediately subjected to CPR. The treatment group animals were administered 15 mg/kg UTI at the onset of resuscitation. The mortality rate in the two groups was recorded at 24 h post-resuscitation. In addition, neurological function was evaluated at 24, 48 and 72 h post-resuscitation using a neurological deficit scale (NDS). Furthermore, the effects of UTI on the Toll-like receptor 4 (TLR4) signaling pathway in brain tissues were determined by assessing TLR4 mRNA expression, nuclear factor (NF)-κB activity and tumor necrosis factor (TNF)-α and interleukin (IL)-6 levels at 1, 3, 6, 12, 24, 48 and 72 h post-resuscitation. After 24 h, the mortality rate significantly decreased in the treatment group when compared with the control animals (10 vs. 30%; P<0.05). Additionally, an overt improvement was observed in the NDS score following UTI treatment when compared with the control (P<0.01). Finally, statistically significant decreases in the levels of TLR4 mRNA expression, NF-κB activity and TNF-α and IL-6 were observed in the treatment group at each time point (P<0.01). Therefore, UTI treatment at the onset of CPR significantly inhibits the TLR4 signaling pathway, thereby alleviating the inflammatory responses following resuscitation and improving neurological function. D.A. Spandidos 2014-10 2014-08-04 /pmc/articles/PMC4151659/ /pubmed/25187844 http://dx.doi.org/10.3892/etm.2014.1876 Text en Copyright © 2014, Spandidos Publications http://creativecommons.org/licenses/by/3.0 This is an open-access article licensed under a Creative Commons Attribution-NonCommercial 3.0 Unported License. The article may be redistributed, reproduced, and reused for non-commercial purposes, provided the original source is properly cited.
spellingShingle Articles
SUI, BO
LI, YONGWANG
MA, LI
Postconditioning improvement effects of ulinastatin on brain injury following cardiopulmonary resuscitation
title Postconditioning improvement effects of ulinastatin on brain injury following cardiopulmonary resuscitation
title_full Postconditioning improvement effects of ulinastatin on brain injury following cardiopulmonary resuscitation
title_fullStr Postconditioning improvement effects of ulinastatin on brain injury following cardiopulmonary resuscitation
title_full_unstemmed Postconditioning improvement effects of ulinastatin on brain injury following cardiopulmonary resuscitation
title_short Postconditioning improvement effects of ulinastatin on brain injury following cardiopulmonary resuscitation
title_sort postconditioning improvement effects of ulinastatin on brain injury following cardiopulmonary resuscitation
topic Articles
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4151659/
https://www.ncbi.nlm.nih.gov/pubmed/25187844
http://dx.doi.org/10.3892/etm.2014.1876
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