Elevation of HO-1 Expression Mitigates Intestinal Ischemia-Reperfusion Injury and Restores Tight Junction Function in a Rat Liver Transplantation Model
Aims. This study was aimed at investigating whether elevation of heme oxygenase-1 (HO-1) expression could lead to restoring intestinal tight junction (TJ) function in a rat liver transplantation model. Methods. Intestinal mucosa injury was induced by orthotopic autologous liver transplantation (OALT...
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| creator | Hei, Ziqing Li, Xi Jin, Yi Xia, Hua Yao, Weifeng Chi, Xinjin Cai, Jun |
| description | Aims. This study was aimed at investigating whether elevation of heme oxygenase-1 (HO-1) expression could lead to restoring intestinal tight junction (TJ) function in a rat liver transplantation model. Methods. Intestinal mucosa injury was induced by orthotopic autologous liver transplantation (OALT) on male Sprague-Dawley rats. Hemin (a potent HO-1 activator) and zinc-protoporphyrin (ZnPP, a HO-1 competitive inhibitor), were separately administered in selected groups before OALT. The serum and intestinal mucosa samples were collected at 8 hours after the operation for analysis. Results. Hemin pretreatment significantly reduced the inflammation and oxidative stress in the mucosal tissue after OALT by elevating HO-1 protein expression, while ZnPP pretreatment aggravated the OALT mucosa injury. Meanwhile, the restriction on the expression of tight junction proteins zonula occludens-1 and occludin was removed after hemin pretreatment. These molecular events led to significant improvement on intestinal barrier function, which was proved to be through increasing nuclear translocation of nuclear factor-E2-related factor 2 (Nrf2) and reducing nuclear translocation of nuclear factor kappa-B (NF-κB) in intestinal injured mucosa. Summary. Our study demonstrated that elevation of HO-1 expression reduced the OALT-induced intestinal mucosa injury and TJ dysfunction. The HO-1 protective function was likely mediated through its effects of anti-inflammation and antioxidative stress. |
| doi_str_mv | 10.1155/2015/986075 |
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This study was aimed at investigating whether elevation of heme oxygenase-1 (HO-1) expression could lead to restoring intestinal tight junction (TJ) function in a rat liver transplantation model. Methods. Intestinal mucosa injury was induced by orthotopic autologous liver transplantation (OALT) on male Sprague-Dawley rats. Hemin (a potent HO-1 activator) and zinc-protoporphyrin (ZnPP, a HO-1 competitive inhibitor), were separately administered in selected groups before OALT. The serum and intestinal mucosa samples were collected at 8 hours after the operation for analysis. Results. Hemin pretreatment significantly reduced the inflammation and oxidative stress in the mucosal tissue after OALT by elevating HO-1 protein expression, while ZnPP pretreatment aggravated the OALT mucosa injury. Meanwhile, the restriction on the expression of tight junction proteins zonula occludens-1 and occludin was removed after hemin pretreatment. These molecular events led to significant improvement on intestinal barrier function, which was proved to be through increasing nuclear translocation of nuclear factor-E2-related factor 2 (Nrf2) and reducing nuclear translocation of nuclear factor kappa-B (NF-κB) in intestinal injured mucosa. Summary. Our study demonstrated that elevation of HO-1 expression reduced the OALT-induced intestinal mucosa injury and TJ dysfunction. The HO-1 protective function was likely mediated through its effects of anti-inflammation and antioxidative stress.</description><identifier>ISSN: 1942-0900</identifier><identifier>EISSN: 1942-0994</identifier><identifier>DOI: 10.1155/2015/986075</identifier><identifier>PMID: 26064429</identifier><language>eng</language><publisher>Cairo, Egypt: Hindawi Publishing Corporation</publisher><subject>Animals ; Apoptosis - drug effects ; Caspase 3 - metabolism ; Disease Models, Animal ; Heme Oxygenase-1 - chemistry ; Heme Oxygenase-1 - genetics ; Heme Oxygenase-1 - metabolism ; Hemin - pharmacology ; Inflammation - prevention & control ; Intestinal Mucosa - drug effects ; Intestinal Mucosa - metabolism ; Intestines ; Liver ; Liver Transplantation - adverse effects ; Male ; Malondialdehyde - metabolism ; Mortality ; NF-E2-Related Factor 2 - metabolism ; Occludin - metabolism ; Oxidases ; Oxidative Stress - drug effects ; Physiological aspects ; Protoporphyrins - pharmacology ; Rats ; Rats, Sprague-Dawley ; Reperfusion Injury - etiology ; Reperfusion Injury - metabolism ; Rodents ; Small intestine ; Studies ; Superoxide Dismutase - metabolism ; Tight Junctions - metabolism ; Transplantation ; Transplants & implants ; Zonula Occludens-1 Protein - metabolism</subject><ispartof>Oxidative medicine and cellular longevity, 2015-01, Vol.2015 (2015), p.1-12</ispartof><rights>Copyright © 2015 Xinjin Chi et al.</rights><rights>COPYRIGHT 2015 John Wiley & Sons, Inc.</rights><rights>Copyright © 2015 Xinjin Chi et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.</rights><rights>Copyright © 2015 Xinjin Chi et al. 2015</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c561t-375cc528a944f33468f89e9ccd0342e4345baf0c5bbfb29c4e5dc6f33639f1343</citedby><cites>FETCH-LOGICAL-c561t-375cc528a944f33468f89e9ccd0342e4345baf0c5bbfb29c4e5dc6f33639f1343</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/PMC4441991/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC4441991/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,727,780,784,885,27923,27924,53790,53792</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/26064429$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><contributor>Grune, Tilman</contributor><creatorcontrib>Hei, Ziqing</creatorcontrib><creatorcontrib>Li, Xi</creatorcontrib><creatorcontrib>Jin, Yi</creatorcontrib><creatorcontrib>Xia, Hua</creatorcontrib><creatorcontrib>Yao, Weifeng</creatorcontrib><creatorcontrib>Chi, Xinjin</creatorcontrib><creatorcontrib>Cai, Jun</creatorcontrib><title>Elevation of HO-1 Expression Mitigates Intestinal Ischemia-Reperfusion Injury and Restores Tight Junction Function in a Rat Liver Transplantation Model</title><title>Oxidative medicine and cellular longevity</title><addtitle>Oxid Med Cell Longev</addtitle><description>Aims. This study was aimed at investigating whether elevation of heme oxygenase-1 (HO-1) expression could lead to restoring intestinal tight junction (TJ) function in a rat liver transplantation model. Methods. Intestinal mucosa injury was induced by orthotopic autologous liver transplantation (OALT) on male Sprague-Dawley rats. Hemin (a potent HO-1 activator) and zinc-protoporphyrin (ZnPP, a HO-1 competitive inhibitor), were separately administered in selected groups before OALT. The serum and intestinal mucosa samples were collected at 8 hours after the operation for analysis. Results. Hemin pretreatment significantly reduced the inflammation and oxidative stress in the mucosal tissue after OALT by elevating HO-1 protein expression, while ZnPP pretreatment aggravated the OALT mucosa injury. Meanwhile, the restriction on the expression of tight junction proteins zonula occludens-1 and occludin was removed after hemin pretreatment. These molecular events led to significant improvement on intestinal barrier function, which was proved to be through increasing nuclear translocation of nuclear factor-E2-related factor 2 (Nrf2) and reducing nuclear translocation of nuclear factor kappa-B (NF-κB) in intestinal injured mucosa. Summary. Our study demonstrated that elevation of HO-1 expression reduced the OALT-induced intestinal mucosa injury and TJ dysfunction. The HO-1 protective function was likely mediated through its effects of anti-inflammation and antioxidative stress.</description><subject>Animals</subject><subject>Apoptosis - drug effects</subject><subject>Caspase 3 - metabolism</subject><subject>Disease Models, Animal</subject><subject>Heme Oxygenase-1 - chemistry</subject><subject>Heme Oxygenase-1 - genetics</subject><subject>Heme Oxygenase-1 - metabolism</subject><subject>Hemin - pharmacology</subject><subject>Inflammation - prevention & control</subject><subject>Intestinal Mucosa - drug effects</subject><subject>Intestinal Mucosa - metabolism</subject><subject>Intestines</subject><subject>Liver</subject><subject>Liver Transplantation - adverse effects</subject><subject>Male</subject><subject>Malondialdehyde - metabolism</subject><subject>Mortality</subject><subject>NF-E2-Related Factor 2 - metabolism</subject><subject>Occludin - metabolism</subject><subject>Oxidases</subject><subject>Oxidative Stress - drug effects</subject><subject>Physiological aspects</subject><subject>Protoporphyrins - 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drug effects</topic><topic>Caspase 3 - metabolism</topic><topic>Disease Models, Animal</topic><topic>Heme Oxygenase-1 - chemistry</topic><topic>Heme Oxygenase-1 - genetics</topic><topic>Heme Oxygenase-1 - metabolism</topic><topic>Hemin - pharmacology</topic><topic>Inflammation - prevention & control</topic><topic>Intestinal Mucosa - drug effects</topic><topic>Intestinal Mucosa - metabolism</topic><topic>Intestines</topic><topic>Liver</topic><topic>Liver Transplantation - adverse effects</topic><topic>Male</topic><topic>Malondialdehyde - metabolism</topic><topic>Mortality</topic><topic>NF-E2-Related Factor 2 - metabolism</topic><topic>Occludin - metabolism</topic><topic>Oxidases</topic><topic>Oxidative Stress - drug effects</topic><topic>Physiological aspects</topic><topic>Protoporphyrins - pharmacology</topic><topic>Rats</topic><topic>Rats, Sprague-Dawley</topic><topic>Reperfusion Injury - etiology</topic><topic>Reperfusion Injury - metabolism</topic><topic>Rodents</topic><topic>Small intestine</topic><topic>Studies</topic><topic>Superoxide Dismutase - metabolism</topic><topic>Tight Junctions - metabolism</topic><topic>Transplantation</topic><topic>Transplants & implants</topic><topic>Zonula Occludens-1 Protein - metabolism</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Hei, Ziqing</creatorcontrib><creatorcontrib>Li, Xi</creatorcontrib><creatorcontrib>Jin, Yi</creatorcontrib><creatorcontrib>Xia, Hua</creatorcontrib><creatorcontrib>Yao, Weifeng</creatorcontrib><creatorcontrib>Chi, Xinjin</creatorcontrib><creatorcontrib>Cai, Jun</creatorcontrib><collection>الدوريات العلمية والإحصائية - e-Marefa Academic and Statistical Periodicals</collection><collection>معرفة - المحتوى العربي الأكاديمي المتكامل - e-Marefa Academic Complete</collection><collection>Hindawi Publishing Complete</collection><collection>Hindawi Publishing Subscription Journals</collection><collection>Hindawi Publishing Open Access Journals</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>Research Library (Alumni Edition)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>ProQuest Central</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>Research Library Prep</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Research Library</collection><collection>Research Library (Corporate)</collection><collection>Publicly Available Content Database</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>ProQuest Central Basic</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Oxidative medicine and cellular longevity</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Hei, Ziqing</au><au>Li, Xi</au><au>Jin, Yi</au><au>Xia, Hua</au><au>Yao, Weifeng</au><au>Chi, Xinjin</au><au>Cai, Jun</au><au>Grune, Tilman</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Elevation of HO-1 Expression Mitigates Intestinal Ischemia-Reperfusion Injury and Restores Tight Junction Function in a Rat Liver Transplantation Model</atitle><jtitle>Oxidative medicine and cellular longevity</jtitle><addtitle>Oxid Med Cell Longev</addtitle><date>2015-01-01</date><risdate>2015</risdate><volume>2015</volume><issue>2015</issue><spage>1</spage><epage>12</epage><pages>1-12</pages><issn>1942-0900</issn><eissn>1942-0994</eissn><abstract>Aims. This study was aimed at investigating whether elevation of heme oxygenase-1 (HO-1) expression could lead to restoring intestinal tight junction (TJ) function in a rat liver transplantation model. Methods. Intestinal mucosa injury was induced by orthotopic autologous liver transplantation (OALT) on male Sprague-Dawley rats. Hemin (a potent HO-1 activator) and zinc-protoporphyrin (ZnPP, a HO-1 competitive inhibitor), were separately administered in selected groups before OALT. The serum and intestinal mucosa samples were collected at 8 hours after the operation for analysis. Results. Hemin pretreatment significantly reduced the inflammation and oxidative stress in the mucosal tissue after OALT by elevating HO-1 protein expression, while ZnPP pretreatment aggravated the OALT mucosa injury. Meanwhile, the restriction on the expression of tight junction proteins zonula occludens-1 and occludin was removed after hemin pretreatment. These molecular events led to significant improvement on intestinal barrier function, which was proved to be through increasing nuclear translocation of nuclear factor-E2-related factor 2 (Nrf2) and reducing nuclear translocation of nuclear factor kappa-B (NF-κB) in intestinal injured mucosa. Summary. Our study demonstrated that elevation of HO-1 expression reduced the OALT-induced intestinal mucosa injury and TJ dysfunction. The HO-1 protective function was likely mediated through its effects of anti-inflammation and antioxidative stress.</abstract><cop>Cairo, Egypt</cop><pub>Hindawi Publishing Corporation</pub><pmid>26064429</pmid><doi>10.1155/2015/986075</doi><tpages>12</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Animals Apoptosis - drug effects Caspase 3 - metabolism Disease Models, Animal Heme Oxygenase-1 - chemistry Heme Oxygenase-1 - genetics Heme Oxygenase-1 - metabolism Hemin - pharmacology Inflammation - prevention & control Intestinal Mucosa - drug effects Intestinal Mucosa - metabolism Intestines Liver Liver Transplantation - adverse effects Male Malondialdehyde - metabolism Mortality NF-E2-Related Factor 2 - metabolism Occludin - metabolism Oxidases Oxidative Stress - drug effects Physiological aspects Protoporphyrins - pharmacology Rats Rats, Sprague-Dawley Reperfusion Injury - etiology Reperfusion Injury - metabolism Rodents Small intestine Studies Superoxide Dismutase - metabolism Tight Junctions - metabolism Transplantation Transplants & implants Zonula Occludens-1 Protein - metabolism |
| title | Elevation of HO-1 Expression Mitigates Intestinal Ischemia-Reperfusion Injury and Restores Tight Junction Function in a Rat Liver Transplantation Model |
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