Insulin alleviates the inflammatory response and oxidative stress injury in cerebral tissues in septic rats

Sepsis-associated encephalopathy (SAE) is a diffuse brain dysfunction that occurs secondary to infection in the body without overt central nervous system (CNS) infection. SAE is frequently encountered in critically ill patients in intensive care units and can be detected in up to 50-70% of septic pa...

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Published in:Journal of inflammation (London, England) England), 2014-06, Vol.11 (1), p.18-18, Article 18
Main Authors: Chen, Qiyi, Yu, Wenkui, Shi, Jiangliang, Shen, Juanhong, Gao, Tao, Zhang, Juanjuan, Xi, Fengchan, Li, Jieshou, Li, Ning
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Language:English
Subjects:
Brain damage
Care and treatment
Complications and side effects
Diagnosis
Glucose
Health aspects
Insulin
Medical research
Medicine, Experimental
Mortality
Nervous system
Oxidative stress
Patient outcomes
Physiological aspects
Risk factors
Rodents
Sepsis
Studies
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cited_by cdi_FETCH-LOGICAL-b613t-49105773032a3cf4158629aea900f3443a556e28a9eee5dcb68a95ec5964ad403
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container_issue 1
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container_title Journal of inflammation (London, England)
container_volume 11
creator Chen, Qiyi
Yu, Wenkui
Shi, Jiangliang
Shen, Juanhong
Gao, Tao
Zhang, Juanjuan
Xi, Fengchan
Li, Jieshou
Li, Ning
description Sepsis-associated encephalopathy (SAE) is a diffuse brain dysfunction that occurs secondary to infection in the body without overt central nervous system (CNS) infection. SAE is frequently encountered in critically ill patients in intensive care units and can be detected in up to 50-70% of septic patients. Previous studies have demonstrated that inflammatory cytokine release and oxidative stress injury are major pathophysiological mechanisms of SAE in critically ill patients. However, there are no effective strategies for the treatment of SAE. Insulin has important immunomodulatory effects and protective effects against oxidative stress injury in the peripheral organs of septic patients. However, very few studies of the possible effects of insulin in cerebral tissues of septic patients have been reported. Therefore, in this study, we aimed to explore whether insulin therapy can inhibit cytokine production (IL-1, IL-6, and TNF-a) and oxidative stress injury of the brain tissue in septic rats. We observed that the protein concentrations of IL-1, IL-6, and TNF-а, in addition to MDA and H2O2 were notably increased, inversely SOD, and GSH were sigificantly decreased in cortex, hippocampus, and hypothalamus of septic rats. Furthermore, the levels of S100 and NSE significantly increased. After 6 hours of insulin therapy, we found that the cytokine concentrations notably decreased and oxidative stress injuries in the cortex, hypothalamus, and hippocampus were alleviated in septic rats. In addition, the S100 and NSE levels significantly decreased. We concluded that insulin can inhibit the production of inflammatory cytokines and the oxidative stress response, thereby improving brain tissue damage.
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SAE is frequently encountered in critically ill patients in intensive care units and can be detected in up to 50-70% of septic patients. Previous studies have demonstrated that inflammatory cytokine release and oxidative stress injury are major pathophysiological mechanisms of SAE in critically ill patients. However, there are no effective strategies for the treatment of SAE. Insulin has important immunomodulatory effects and protective effects against oxidative stress injury in the peripheral organs of septic patients. However, very few studies of the possible effects of insulin in cerebral tissues of septic patients have been reported. Therefore, in this study, we aimed to explore whether insulin therapy can inhibit cytokine production (IL-1, IL-6, and TNF-a) and oxidative stress injury of the brain tissue in septic rats. We observed that the protein concentrations of IL-1, IL-6, and TNF-а, in addition to MDA and H2O2 were notably increased, inversely SOD, and GSH were sigificantly decreased in cortex, hippocampus, and hypothalamus of septic rats. Furthermore, the levels of S100 and NSE significantly increased. After 6 hours of insulin therapy, we found that the cytokine concentrations notably decreased and oxidative stress injuries in the cortex, hypothalamus, and hippocampus were alleviated in septic rats. In addition, the S100 and NSE levels significantly decreased. We concluded that insulin can inhibit the production of inflammatory cytokines and the oxidative stress response, thereby improving brain tissue damage.</description><identifier>ISSN: 1476-9255</identifier><identifier>EISSN: 1476-9255</identifier><identifier>DOI: 10.1186/1476-9255-11-18</identifier><identifier>PMID: 25093012</identifier><language>eng</language><publisher>England: BioMed Central Ltd</publisher><subject>Brain damage ; Care and treatment ; Complications and side effects ; Diagnosis ; Glucose ; Health aspects ; Insulin ; Medical research ; Medicine, Experimental ; Mortality ; Nervous system ; Oxidative stress ; Patient outcomes ; Physiological aspects ; Risk factors ; Rodents ; Sepsis ; Studies</subject><ispartof>Journal of inflammation (London, England), 2014-06, Vol.11 (1), p.18-18, Article 18</ispartof><rights>COPYRIGHT 2014 BioMed Central Ltd.</rights><rights>2014 Chen et al.; licensee BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly credited.</rights><rights>Copyright © 2014 Chen et al.; licensee BioMed Central Ltd. 2014 Chen et al.; licensee BioMed Central Ltd.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-b613t-49105773032a3cf4158629aea900f3443a556e28a9eee5dcb68a95ec5964ad403</citedby><cites>FETCH-LOGICAL-b613t-49105773032a3cf4158629aea900f3443a556e28a9eee5dcb68a95ec5964ad403</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC4108965/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.proquest.com/docview/1548368851?pq-origsite=primo$$EHTML$$P50$$Gproquest$$Hfree_for_read</linktohtml><link.rule.ids>230,315,733,786,790,891,25783,27957,27958,37047,37048,44625,53827,53829</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/25093012$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Chen, Qiyi</creatorcontrib><creatorcontrib>Yu, Wenkui</creatorcontrib><creatorcontrib>Shi, Jiangliang</creatorcontrib><creatorcontrib>Shen, Juanhong</creatorcontrib><creatorcontrib>Gao, Tao</creatorcontrib><creatorcontrib>Zhang, Juanjuan</creatorcontrib><creatorcontrib>Xi, Fengchan</creatorcontrib><creatorcontrib>Li, Jieshou</creatorcontrib><creatorcontrib>Li, Ning</creatorcontrib><title>Insulin alleviates the inflammatory response and oxidative stress injury in cerebral tissues in septic rats</title><title>Journal of inflammation (London, England)</title><addtitle>J Inflamm (Lond)</addtitle><description>Sepsis-associated encephalopathy (SAE) is a diffuse brain dysfunction that occurs secondary to infection in the body without overt central nervous system (CNS) infection. 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We observed that the protein concentrations of IL-1, IL-6, and TNF-а, in addition to MDA and H2O2 were notably increased, inversely SOD, and GSH were sigificantly decreased in cortex, hippocampus, and hypothalamus of septic rats. Furthermore, the levels of S100 and NSE significantly increased. After 6 hours of insulin therapy, we found that the cytokine concentrations notably decreased and oxidative stress injuries in the cortex, hypothalamus, and hippocampus were alleviated in septic rats. In addition, the S100 and NSE levels significantly decreased. 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We observed that the protein concentrations of IL-1, IL-6, and TNF-а, in addition to MDA and H2O2 were notably increased, inversely SOD, and GSH were sigificantly decreased in cortex, hippocampus, and hypothalamus of septic rats. Furthermore, the levels of S100 and NSE significantly increased. After 6 hours of insulin therapy, we found that the cytokine concentrations notably decreased and oxidative stress injuries in the cortex, hypothalamus, and hippocampus were alleviated in septic rats. In addition, the S100 and NSE levels significantly decreased. We concluded that insulin can inhibit the production of inflammatory cytokines and the oxidative stress response, thereby improving brain tissue damage.</abstract><cop>England</cop><pub>BioMed Central Ltd</pub><pmid>25093012</pmid><doi>10.1186/1476-9255-11-18</doi><tpages>1</tpages><oa>free_for_read</oa></addata></record>
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subjects Brain damage
Care and treatment
Complications and side effects
Diagnosis
Glucose
Health aspects
Insulin
Medical research
Medicine, Experimental
Mortality
Nervous system
Oxidative stress
Patient outcomes
Physiological aspects
Risk factors
Rodents
Sepsis
Studies
title Insulin alleviates the inflammatory response and oxidative stress injury in cerebral tissues in septic rats
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