Dimethyl sulfoxide inhibits zymosan-induced intestinal inflammation and barrier dysfunction

AIM: To investigate whether dimethyl sulfoxide(DMSO) inhibits gut inflammation and barrier dysfunction following zymosan-induced systemic inflammatoryresponse syndrome and multiple organ dysfunction syndrome.METHODS: Sprague-Dawley rats were randomly divided into four groups: sham with administratio...

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Veröffentlicht in:World journal of gastroenterology : WJG 2015-10, Vol.21 (38), p.10853-10865
Hauptverfasser: Li, Yu-Meng, Wang, Hai-Bin, Zheng, Jin-Guang, Bai, Xiao-Dong, Zhao, Zeng-Kai, Li, Jing-Yuan, Hu, Sen
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container_end_page 10865
container_issue 38
container_start_page 10853
container_title World journal of gastroenterology : WJG
container_volume 21
creator Li, Yu-Meng
Wang, Hai-Bin
Zheng, Jin-Guang
Bai, Xiao-Dong
Zhao, Zeng-Kai
Li, Jing-Yuan
Hu, Sen
description AIM: To investigate whether dimethyl sulfoxide(DMSO) inhibits gut inflammation and barrier dysfunction following zymosan-induced systemic inflammatoryresponse syndrome and multiple organ dysfunction syndrome.METHODS: Sprague-Dawley rats were randomly divided into four groups: sham with administration of normal saline(SS group); sham with administration of DMSO(SD group); zymosan with administration of normal saline(ZS group); and zymosan with administration of DMSO(ZD group). Each group contained three subgroups according to 4 h,8 h,and 24 h after surgery. At 4 h,8 h,and 24 h after intraperitoneal injection of zymosan(750 mg/kg),the levels of intestinal inflammatory cytokines [tumor necrosis factor-alpha(TNF-α) and interleukin(IL)-10] and oxides(myeloperoxidase,malonaldehyde,and superoxide dismutase) were examined. The levels of diamine oxidase(DAO) in plasma and intestinal mucosal blood flow(IMBF) were determined. Intestinal injury was also evaluated using an intestinal histological score and apoptosis of intestinal epithelial cells was determined by deoxynucleotidyl transferase d UTP nick end labeling(TUNEL) assay. The intestinal epithelial tight junction protein,ZO-1,was observed by immunofluorescence.RESULTS: DMSO decreased TNF-α and increased IL-10 levels in the intestine compared with the ZS group at the corresponding time points. The activity of intestinal myeloperoxidase in the ZS group was higher than that in the ZD group 24 h after zymosan administration(P < 0.05). DMSO decreased the content of malondialdehyde(MDA) and increased the activity of superoxide dehydrogenase(SOD) 24 h after zymosan administration. The IMBF was lowest at 24 h and was 49.34% and 58.26% in the ZS group and ZD group,respectively(P < 0.05). DMSO alleviated injury in intestinal villi,and the gut injury score was significantly lower than the ZS group(3.6 ± 0.2 vs 4.2 ± 0.3,P < 0.05). DMSO decreased the level of DAO in plasma compared with the ZS group(65.1 ± 4.7 U/L vs 81.1 ± 5.0 U/L,P < 0.05). DMSO significantly preserved ZO-1 protein expression and localization 24 h after zymosan administration. The TUNEL analysis indicated that the number of apoptotic intestinal cells in the ZS group was much higher than the ZD group(P < 0.05).CONCLUSION: DMSO inhibited intestinal cytokines and protected against zymosan-induced gut barrier dysfunction.
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Each group contained three subgroups according to 4 h,8 h,and 24 h after surgery. At 4 h,8 h,and 24 h after intraperitoneal injection of zymosan(750 mg/kg),the levels of intestinal inflammatory cytokines [tumor necrosis factor-alpha(TNF-α) and interleukin(IL)-10] and oxides(myeloperoxidase,malonaldehyde,and superoxide dismutase) were examined. The levels of diamine oxidase(DAO) in plasma and intestinal mucosal blood flow(IMBF) were determined. Intestinal injury was also evaluated using an intestinal histological score and apoptosis of intestinal epithelial cells was determined by deoxynucleotidyl transferase d UTP nick end labeling(TUNEL) assay. The intestinal epithelial tight junction protein,ZO-1,was observed by immunofluorescence.RESULTS: DMSO decreased TNF-α and increased IL-10 levels in the intestine compared with the ZS group at the corresponding time points. The activity of intestinal myeloperoxidase in the ZS group was higher than that in the ZD group 24 h after zymosan administration(P &amp;lt; 0.05). DMSO decreased the content of malondialdehyde(MDA) and increased the activity of superoxide dehydrogenase(SOD) 24 h after zymosan administration. The IMBF was lowest at 24 h and was 49.34% and 58.26% in the ZS group and ZD group,respectively(P &amp;lt; 0.05). DMSO alleviated injury in intestinal villi,and the gut injury score was significantly lower than the ZS group(3.6 ± 0.2 vs 4.2 ± 0.3,P &amp;lt; 0.05). DMSO decreased the level of DAO in plasma compared with the ZS group(65.1 ± 4.7 U/L vs 81.1 ± 5.0 U/L,P &amp;lt; 0.05). DMSO significantly preserved ZO-1 protein expression and localization 24 h after zymosan administration. The TUNEL analysis indicated that the number of apoptotic intestinal cells in the ZS group was much higher than the ZD group(P &amp;lt; 0.05).CONCLUSION: DMSO inhibited intestinal cytokines and protected against zymosan-induced gut barrier dysfunction.</description><identifier>ISSN: 1007-9327</identifier><identifier>EISSN: 2219-2840</identifier><identifier>DOI: 10.3748/wjg.v21.i38.10853</identifier><identifier>PMID: 26478676</identifier><language>eng</language><publisher>United States: Baishideng Publishing Group Inc</publisher><subject>Amine Oxidase (Copper-Containing) - blood ; Animals ; Apoptosis - drug effects ; Basic Study ; Dimethyl ; Dimethyl Sulfoxide - pharmacology ; Enteritis - chemically induced ; Enteritis - drug therapy ; Enteritis - metabolism ; Enteritis - pathology ; Free Radical Scavengers - pharmacology ; Interleukin-10 - metabolism ; Intestinal Mucosa - blood supply ; Intestinal Mucosa - drug effects ; Intestinal Mucosa - metabolism ; Intestinal Mucosa - pathology ; Male ; Malondialdehyde - metabolism ; Multiple Organ Failure - chemically induced ; Rats ; Rats, Sprague-Dawley ; Regional Blood Flow - drug effects ; sulfoxide;Zymosan;Inflammation;Intestinal ; Superoxide Dismutase - metabolism ; Systemic Inflammatory Response Syndrome - chemically induced ; Tight Junctions - drug effects ; Tumor Necrosis Factor-alpha - metabolism ; Zonula Occludens-1 Protein - metabolism ; Zymosan</subject><ispartof>World journal of gastroenterology : WJG, 2015-10, Vol.21 (38), p.10853-10865</ispartof><rights>The Author(s) 2015. 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All rights reserved. 2015</rights><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c443t-6aaa329c23cb795ae57e0cfbcecabccb02aa15ee0a9fabd65f93f5c193edfb313</citedby><cites>FETCH-LOGICAL-c443t-6aaa329c23cb795ae57e0cfbcecabccb02aa15ee0a9fabd65f93f5c193edfb313</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Uhttp://image.cqvip.com/vip1000/qk/84123X/84123X.jpg</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC4600586/pdf/$$EPDF$$P50$$Gpubmedcentral$$H</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC4600586/$$EHTML$$P50$$Gpubmedcentral$$H</linktohtml><link.rule.ids>230,315,728,781,785,886,27926,27927,53793,53795</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/26478676$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Li, Yu-Meng</creatorcontrib><creatorcontrib>Wang, Hai-Bin</creatorcontrib><creatorcontrib>Zheng, Jin-Guang</creatorcontrib><creatorcontrib>Bai, Xiao-Dong</creatorcontrib><creatorcontrib>Zhao, Zeng-Kai</creatorcontrib><creatorcontrib>Li, Jing-Yuan</creatorcontrib><creatorcontrib>Hu, Sen</creatorcontrib><title>Dimethyl sulfoxide inhibits zymosan-induced intestinal inflammation and barrier dysfunction</title><title>World journal of gastroenterology : WJG</title><addtitle>World Journal of Gastroenterology</addtitle><description>AIM: To investigate whether dimethyl sulfoxide(DMSO) inhibits gut inflammation and barrier dysfunction following zymosan-induced systemic inflammatoryresponse syndrome and multiple organ dysfunction syndrome.METHODS: Sprague-Dawley rats were randomly divided into four groups: sham with administration of normal saline(SS group); sham with administration of DMSO(SD group); zymosan with administration of normal saline(ZS group); and zymosan with administration of DMSO(ZD group). Each group contained three subgroups according to 4 h,8 h,and 24 h after surgery. At 4 h,8 h,and 24 h after intraperitoneal injection of zymosan(750 mg/kg),the levels of intestinal inflammatory cytokines [tumor necrosis factor-alpha(TNF-α) and interleukin(IL)-10] and oxides(myeloperoxidase,malonaldehyde,and superoxide dismutase) were examined. The levels of diamine oxidase(DAO) in plasma and intestinal mucosal blood flow(IMBF) were determined. Intestinal injury was also evaluated using an intestinal histological score and apoptosis of intestinal epithelial cells was determined by deoxynucleotidyl transferase d UTP nick end labeling(TUNEL) assay. The intestinal epithelial tight junction protein,ZO-1,was observed by immunofluorescence.RESULTS: DMSO decreased TNF-α and increased IL-10 levels in the intestine compared with the ZS group at the corresponding time points. The activity of intestinal myeloperoxidase in the ZS group was higher than that in the ZD group 24 h after zymosan administration(P &amp;lt; 0.05). DMSO decreased the content of malondialdehyde(MDA) and increased the activity of superoxide dehydrogenase(SOD) 24 h after zymosan administration. The IMBF was lowest at 24 h and was 49.34% and 58.26% in the ZS group and ZD group,respectively(P &amp;lt; 0.05). DMSO alleviated injury in intestinal villi,and the gut injury score was significantly lower than the ZS group(3.6 ± 0.2 vs 4.2 ± 0.3,P &amp;lt; 0.05). DMSO decreased the level of DAO in plasma compared with the ZS group(65.1 ± 4.7 U/L vs 81.1 ± 5.0 U/L,P &amp;lt; 0.05). DMSO significantly preserved ZO-1 protein expression and localization 24 h after zymosan administration. The TUNEL analysis indicated that the number of apoptotic intestinal cells in the ZS group was much higher than the ZD group(P &amp;lt; 0.05).CONCLUSION: DMSO inhibited intestinal cytokines and protected against zymosan-induced gut barrier dysfunction.</description><subject>Amine Oxidase (Copper-Containing) - blood</subject><subject>Animals</subject><subject>Apoptosis - drug effects</subject><subject>Basic Study</subject><subject>Dimethyl</subject><subject>Dimethyl Sulfoxide - pharmacology</subject><subject>Enteritis - chemically induced</subject><subject>Enteritis - drug therapy</subject><subject>Enteritis - metabolism</subject><subject>Enteritis - pathology</subject><subject>Free Radical Scavengers - pharmacology</subject><subject>Interleukin-10 - metabolism</subject><subject>Intestinal Mucosa - blood supply</subject><subject>Intestinal Mucosa - drug effects</subject><subject>Intestinal Mucosa - metabolism</subject><subject>Intestinal Mucosa - pathology</subject><subject>Male</subject><subject>Malondialdehyde - metabolism</subject><subject>Multiple Organ Failure - chemically induced</subject><subject>Rats</subject><subject>Rats, Sprague-Dawley</subject><subject>Regional Blood Flow - drug effects</subject><subject>sulfoxide;Zymosan;Inflammation;Intestinal</subject><subject>Superoxide Dismutase - metabolism</subject><subject>Systemic Inflammatory Response Syndrome - chemically induced</subject><subject>Tight Junctions - drug effects</subject><subject>Tumor Necrosis Factor-alpha - metabolism</subject><subject>Zonula Occludens-1 Protein - metabolism</subject><subject>Zymosan</subject><issn>1007-9327</issn><issn>2219-2840</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2015</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpVkU9v1DAQxS0EokvhA3BBOXLJ4r-JfUFChQJSJS7tiYM1duxdV4nd2klh--nxtsuqncuM_N482_oh9J7gNeu5_PTnerO-o2QdmFwTLAV7gVaUEtVSyfFLtCIY961itD9Bb0q5xpgyJuhrdEI73suu71bo99cwuXm7G5uyjD79DYNrQtwGE-bS3O-mVCC2IQ6LdUMVZlfmEGGsox9hmmAOKTYQh8ZAzsHlZtgVv0S7P3-LXnkYi3t36Kfo6vzb5dmP9uLX959nXy5ayzmb2w4AGFWWMmt6JcCJ3mHrjXUWjLUGUwAinMOgPJihE14xLyxRzA3eMMJO0efH3JvFTG6wLs4ZRn2TwwR5pxME_VyJYas36U7zDmMhuxrw8RCQ0-1Sv6inUKwbR4guLUWTnnLaEcFltZJHq82plOz88RqC9R6KrlB0haIrFP0Ape58ePq-48Z_CtXADqHbFDe3IW6OHoXlvpTAXHIlmCCie5g4-weAQ545</recordid><startdate>20151014</startdate><enddate>20151014</enddate><creator>Li, Yu-Meng</creator><creator>Wang, Hai-Bin</creator><creator>Zheng, Jin-Guang</creator><creator>Bai, Xiao-Dong</creator><creator>Zhao, Zeng-Kai</creator><creator>Li, Jing-Yuan</creator><creator>Hu, Sen</creator><general>Baishideng Publishing Group Inc</general><scope>2RA</scope><scope>92L</scope><scope>CQIGP</scope><scope>W91</scope><scope>~WA</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>20151014</creationdate><title>Dimethyl sulfoxide inhibits zymosan-induced intestinal inflammation and barrier dysfunction</title><author>Li, Yu-Meng ; 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sham with administration of DMSO(SD group); zymosan with administration of normal saline(ZS group); and zymosan with administration of DMSO(ZD group). Each group contained three subgroups according to 4 h,8 h,and 24 h after surgery. At 4 h,8 h,and 24 h after intraperitoneal injection of zymosan(750 mg/kg),the levels of intestinal inflammatory cytokines [tumor necrosis factor-alpha(TNF-α) and interleukin(IL)-10] and oxides(myeloperoxidase,malonaldehyde,and superoxide dismutase) were examined. The levels of diamine oxidase(DAO) in plasma and intestinal mucosal blood flow(IMBF) were determined. Intestinal injury was also evaluated using an intestinal histological score and apoptosis of intestinal epithelial cells was determined by deoxynucleotidyl transferase d UTP nick end labeling(TUNEL) assay. The intestinal epithelial tight junction protein,ZO-1,was observed by immunofluorescence.RESULTS: DMSO decreased TNF-α and increased IL-10 levels in the intestine compared with the ZS group at the corresponding time points. The activity of intestinal myeloperoxidase in the ZS group was higher than that in the ZD group 24 h after zymosan administration(P &amp;lt; 0.05). DMSO decreased the content of malondialdehyde(MDA) and increased the activity of superoxide dehydrogenase(SOD) 24 h after zymosan administration. The IMBF was lowest at 24 h and was 49.34% and 58.26% in the ZS group and ZD group,respectively(P &amp;lt; 0.05). DMSO alleviated injury in intestinal villi,and the gut injury score was significantly lower than the ZS group(3.6 ± 0.2 vs 4.2 ± 0.3,P &amp;lt; 0.05). DMSO decreased the level of DAO in plasma compared with the ZS group(65.1 ± 4.7 U/L vs 81.1 ± 5.0 U/L,P &amp;lt; 0.05). DMSO significantly preserved ZO-1 protein expression and localization 24 h after zymosan administration. The TUNEL analysis indicated that the number of apoptotic intestinal cells in the ZS group was much higher than the ZD group(P &amp;lt; 0.05).CONCLUSION: DMSO inhibited intestinal cytokines and protected against zymosan-induced gut barrier dysfunction.</abstract><cop>United States</cop><pub>Baishideng Publishing Group Inc</pub><pmid>26478676</pmid><doi>10.3748/wjg.v21.i38.10853</doi><tpages>13</tpages><oa>free_for_read</oa></addata></record>
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subjects Amine Oxidase (Copper-Containing) - blood
Animals
Apoptosis - drug effects
Basic Study
Dimethyl
Dimethyl Sulfoxide - pharmacology
Enteritis - chemically induced
Enteritis - drug therapy
Enteritis - metabolism
Enteritis - pathology
Free Radical Scavengers - pharmacology
Interleukin-10 - metabolism
Intestinal Mucosa - blood supply
Intestinal Mucosa - drug effects
Intestinal Mucosa - metabolism
Intestinal Mucosa - pathology
Male
Malondialdehyde - metabolism
Multiple Organ Failure - chemically induced
Rats
Rats, Sprague-Dawley
Regional Blood Flow - drug effects
sulfoxide
Zymosan
Inflammation
Intestinal
Superoxide Dismutase - metabolism
Systemic Inflammatory Response Syndrome - chemically induced
Tight Junctions - drug effects
Tumor Necrosis Factor-alpha - metabolism
Zonula Occludens-1 Protein - metabolism
Zymosan
title Dimethyl sulfoxide inhibits zymosan-induced intestinal inflammation and barrier dysfunction
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