Heme oxygenase-1 overexpression increases liver injury after bile duct ligation in rats
To investigate the effects of heme oxygenase-1 (HO-1) against oxidant-induced injury caused by bile duct ligation (BDL). Either cobalt protoporphyrin (CoPP), a HO-1 inducer, or saline were injected intraperitoneally in male SD-rats. Three days later, BDL or sham-operations were performed. Rats were...
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| Veröffentlicht in: | World journal of gastroenterology : WJG 2007-07, Vol.13 (25), p.3478-3486 |
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| container_title | World journal of gastroenterology : WJG |
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| creator | Froh, Matthias Conzelmann, Lars Walbrun, Peter Netter, Susanne Wiest, Reiner Wheeler, Michael-D Lehnert, Mark Uesugi, Takehiko Scholmerich, Jurgen Thurman, Ronald G |
| description | To investigate the effects of heme oxygenase-1 (HO-1) against oxidant-induced injury caused by bile duct ligation (BDL).
Either cobalt protoporphyrin (CoPP), a HO-1 inducer, or saline were injected intraperitoneally in male SD-rats. Three days later, BDL or sham-operations were performed. Rats were sacrificed 3 wk after BDL and livers were harvested for histology. Fibrosis was evaluated by sirius red staining and image analysis. Alpha-smooth muscular actin, which indicates activation of stellate cells, was detected by immunohistochemical staining, and cytokine and collagen-Ialpha (Col-Ialpha) mRNA expression was detected using RNase protection assays.
Serum alanine transaminase increased 8-fold above normal levels one day after BDL. Surprisingly, enzyme release was not reduced in rats receiving CoPP. Liver fibrosis was evaluated 3 wk after BDL and the sirius red-positive area was found to be increased to about 7.8%. However, in CoPP pretreated rats sirius red-positive areas were increased to about 11.7% after BDL. Collagen-Ialpha and TGF-beta mRNA increased significantly by BDL. Again, this effect was increased by HO-1 overexpression.
Hepatic fibrosis due to BDL is not reduced by the HO-1 inducer CoPP. In contrast, HO-1 overexpression increases liver injury in rats under conditions of experimental chronic cholestasis. |
| doi_str_mv | 10.3748/wjg.v13.i25.3478 |
| format | Article |
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Either cobalt protoporphyrin (CoPP), a HO-1 inducer, or saline were injected intraperitoneally in male SD-rats. Three days later, BDL or sham-operations were performed. Rats were sacrificed 3 wk after BDL and livers were harvested for histology. Fibrosis was evaluated by sirius red staining and image analysis. Alpha-smooth muscular actin, which indicates activation of stellate cells, was detected by immunohistochemical staining, and cytokine and collagen-Ialpha (Col-Ialpha) mRNA expression was detected using RNase protection assays.
Serum alanine transaminase increased 8-fold above normal levels one day after BDL. Surprisingly, enzyme release was not reduced in rats receiving CoPP. Liver fibrosis was evaluated 3 wk after BDL and the sirius red-positive area was found to be increased to about 7.8%. However, in CoPP pretreated rats sirius red-positive areas were increased to about 11.7% after BDL. Collagen-Ialpha and TGF-beta mRNA increased significantly by BDL. Again, this effect was increased by HO-1 overexpression.
Hepatic fibrosis due to BDL is not reduced by the HO-1 inducer CoPP. In contrast, HO-1 overexpression increases liver injury in rats under conditions of experimental chronic cholestasis.</description><identifier>ISSN: 1007-9327</identifier><identifier>EISSN: 2219-2840</identifier><identifier>DOI: 10.3748/wjg.v13.i25.3478</identifier><identifier>PMID: 17659695</identifier><language>eng</language><publisher>United States: Department of Surgery, University of Osaka,Japan</publisher><subject>Actins - analysis ; Alanine Transaminase - blood ; Animals ; Basic Research ; Bile Ducts ; Cholestasis - complications ; Cholestasis - enzymology ; Chronic Disease ; Heme Oxygenase-1 - physiology ; Immunohistochemistry ; Ligation ; Liver - enzymology ; Liver Cirrhosis - etiology ; Male ; Rats ; Rats, Sprague-Dawley ; RNA, Messenger - analysis ; Transforming Growth Factor beta1 - genetics ; Tumor Necrosis Factor-alpha - genetics</subject><ispartof>World journal of gastroenterology : WJG, 2007-07, Vol.13 (25), p.3478-3486</ispartof><rights>Copyright © Wanfang Data Co. Ltd. All Rights Reserved.</rights><rights>2007 Baishideng Publishing Group Inc. All rights reserved. 2007</rights><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c423t-b8c5a9522c88a110f5eb6856d7a03b6f2cd46ab2aa497ea7f3df18703339b2f53</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Uhttp://www.wanfangdata.com.cn/images/PeriodicalImages/wjg/wjg.jpg</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC4146784/pdf/$$EPDF$$P50$$Gpubmedcentral$$H</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC4146784/$$EHTML$$P50$$Gpubmedcentral$$H</linktohtml><link.rule.ids>230,314,727,780,784,885,27924,27925,53791,53793</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/17659695$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Froh, Matthias</creatorcontrib><creatorcontrib>Conzelmann, Lars</creatorcontrib><creatorcontrib>Walbrun, Peter</creatorcontrib><creatorcontrib>Netter, Susanne</creatorcontrib><creatorcontrib>Wiest, Reiner</creatorcontrib><creatorcontrib>Wheeler, Michael-D</creatorcontrib><creatorcontrib>Lehnert, Mark</creatorcontrib><creatorcontrib>Uesugi, Takehiko</creatorcontrib><creatorcontrib>Scholmerich, Jurgen</creatorcontrib><creatorcontrib>Thurman, Ronald G</creatorcontrib><title>Heme oxygenase-1 overexpression increases liver injury after bile duct ligation in rats</title><title>World journal of gastroenterology : WJG</title><addtitle>World J Gastroenterol</addtitle><description>To investigate the effects of heme oxygenase-1 (HO-1) against oxidant-induced injury caused by bile duct ligation (BDL).
Either cobalt protoporphyrin (CoPP), a HO-1 inducer, or saline were injected intraperitoneally in male SD-rats. Three days later, BDL or sham-operations were performed. Rats were sacrificed 3 wk after BDL and livers were harvested for histology. Fibrosis was evaluated by sirius red staining and image analysis. Alpha-smooth muscular actin, which indicates activation of stellate cells, was detected by immunohistochemical staining, and cytokine and collagen-Ialpha (Col-Ialpha) mRNA expression was detected using RNase protection assays.
Serum alanine transaminase increased 8-fold above normal levels one day after BDL. Surprisingly, enzyme release was not reduced in rats receiving CoPP. Liver fibrosis was evaluated 3 wk after BDL and the sirius red-positive area was found to be increased to about 7.8%. However, in CoPP pretreated rats sirius red-positive areas were increased to about 11.7% after BDL. Collagen-Ialpha and TGF-beta mRNA increased significantly by BDL. Again, this effect was increased by HO-1 overexpression.
Hepatic fibrosis due to BDL is not reduced by the HO-1 inducer CoPP. In contrast, HO-1 overexpression increases liver injury in rats under conditions of experimental chronic cholestasis.</description><subject>Actins - analysis</subject><subject>Alanine Transaminase - blood</subject><subject>Animals</subject><subject>Basic Research</subject><subject>Bile Ducts</subject><subject>Cholestasis - complications</subject><subject>Cholestasis - enzymology</subject><subject>Chronic Disease</subject><subject>Heme Oxygenase-1 - physiology</subject><subject>Immunohistochemistry</subject><subject>Ligation</subject><subject>Liver - enzymology</subject><subject>Liver Cirrhosis - etiology</subject><subject>Male</subject><subject>Rats</subject><subject>Rats, Sprague-Dawley</subject><subject>RNA, Messenger - analysis</subject><subject>Transforming Growth Factor beta1 - genetics</subject><subject>Tumor Necrosis Factor-alpha - genetics</subject><issn>1007-9327</issn><issn>2219-2840</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2007</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpVkc1v1DAQxS0EokvhzgnlgLhl68_YuSChqlCkSr204mhNknHwKmsvdrLt_vd4tSs-TtbovXmemR8h7xldCy3N1dNmXO-ZWHuu1kJq84KsOGdtzY2kL8mKUarrVnB9Qd7kvKGUC6H4a3LBdKPaplUr8uMWt1jF58OIATLWrIp7TPi8S5izj6HyoU9YlFxNviil3izpUIGbS9H5Cath6ecijjCf_FWCOb8lrxxMGd-d30vy-PXm4fq2vrv_9v36y13dSy7mujO9glZx3hsDjFGnsGuMagYNVHSN4_0gG-g4gGw1gnZicMxoKoRoO-6UuCSfT7m7pdvi0GOYE0x2l_wW0sFG8PZ_Jfifdox7K5lstJEl4OMp4AmCgzDaTVxSKCPbclxeDsgVZazYPp3_SfHXgnm2W597nCYIGJdsG8OoNMwUIz0Z-xRzTuj-zMKoPUI75toCzRZo9gittHz4d4e_DWdK4je-0pXo</recordid><startdate>20070707</startdate><enddate>20070707</enddate><creator>Froh, Matthias</creator><creator>Conzelmann, Lars</creator><creator>Walbrun, Peter</creator><creator>Netter, Susanne</creator><creator>Wiest, Reiner</creator><creator>Wheeler, Michael-D</creator><creator>Lehnert, Mark</creator><creator>Uesugi, Takehiko</creator><creator>Scholmerich, Jurgen</creator><creator>Thurman, Ronald G</creator><general>Department of Surgery, University of Osaka,Japan</general><general>Department of Internal Medicine,University of Regensburg, Germany</general><general>Department of Urology, University of Mainz,Germany%Department of Internal Medicine,University of Regensburg, Germany%Department of Pharmacology, University of North Carolina, United States%Department of Pharmacology, University of North Carolina, United States</general><general>Department of Surgery, University of Frankfurt,Germany%Department of Pharmacology, University of North Carolina, United States</general><general>Department of Pharmacology, University of North Carolina, United States%Department of Pharmacology, University of North Carolina, United States</general><general>Baishideng Publishing Group Inc</general><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>2B.</scope><scope>4A8</scope><scope>92I</scope><scope>93N</scope><scope>PSX</scope><scope>TCJ</scope><scope>5PM</scope></search><sort><creationdate>20070707</creationdate><title>Heme oxygenase-1 overexpression increases liver injury after bile duct ligation in rats</title><author>Froh, Matthias ; Conzelmann, Lars ; Walbrun, Peter ; Netter, Susanne ; Wiest, Reiner ; Wheeler, Michael-D ; Lehnert, Mark ; Uesugi, Takehiko ; Scholmerich, Jurgen ; Thurman, Ronald G</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c423t-b8c5a9522c88a110f5eb6856d7a03b6f2cd46ab2aa497ea7f3df18703339b2f53</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2007</creationdate><topic>Actins - analysis</topic><topic>Alanine Transaminase - blood</topic><topic>Animals</topic><topic>Basic Research</topic><topic>Bile Ducts</topic><topic>Cholestasis - complications</topic><topic>Cholestasis - enzymology</topic><topic>Chronic Disease</topic><topic>Heme Oxygenase-1 - physiology</topic><topic>Immunohistochemistry</topic><topic>Ligation</topic><topic>Liver - enzymology</topic><topic>Liver Cirrhosis - etiology</topic><topic>Male</topic><topic>Rats</topic><topic>Rats, Sprague-Dawley</topic><topic>RNA, Messenger - analysis</topic><topic>Transforming Growth Factor beta1 - genetics</topic><topic>Tumor Necrosis Factor-alpha - genetics</topic><toplevel>online_resources</toplevel><creatorcontrib>Froh, Matthias</creatorcontrib><creatorcontrib>Conzelmann, Lars</creatorcontrib><creatorcontrib>Walbrun, Peter</creatorcontrib><creatorcontrib>Netter, Susanne</creatorcontrib><creatorcontrib>Wiest, Reiner</creatorcontrib><creatorcontrib>Wheeler, Michael-D</creatorcontrib><creatorcontrib>Lehnert, Mark</creatorcontrib><creatorcontrib>Uesugi, Takehiko</creatorcontrib><creatorcontrib>Scholmerich, Jurgen</creatorcontrib><creatorcontrib>Thurman, Ronald G</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><collection>Wanfang Data Journals - Hong Kong</collection><collection>WANFANG Data Centre</collection><collection>Wanfang Data Journals</collection><collection>万方数据期刊 - 香港版</collection><collection>China Online Journals (COJ)</collection><collection>China Online Journals (COJ)</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>World journal of gastroenterology : WJG</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Froh, Matthias</au><au>Conzelmann, Lars</au><au>Walbrun, Peter</au><au>Netter, Susanne</au><au>Wiest, Reiner</au><au>Wheeler, Michael-D</au><au>Lehnert, Mark</au><au>Uesugi, Takehiko</au><au>Scholmerich, Jurgen</au><au>Thurman, Ronald G</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Heme oxygenase-1 overexpression increases liver injury after bile duct ligation in rats</atitle><jtitle>World journal of gastroenterology : WJG</jtitle><addtitle>World J Gastroenterol</addtitle><date>2007-07-07</date><risdate>2007</risdate><volume>13</volume><issue>25</issue><spage>3478</spage><epage>3486</epage><pages>3478-3486</pages><issn>1007-9327</issn><eissn>2219-2840</eissn><abstract>To investigate the effects of heme oxygenase-1 (HO-1) against oxidant-induced injury caused by bile duct ligation (BDL).
Either cobalt protoporphyrin (CoPP), a HO-1 inducer, or saline were injected intraperitoneally in male SD-rats. Three days later, BDL or sham-operations were performed. Rats were sacrificed 3 wk after BDL and livers were harvested for histology. Fibrosis was evaluated by sirius red staining and image analysis. Alpha-smooth muscular actin, which indicates activation of stellate cells, was detected by immunohistochemical staining, and cytokine and collagen-Ialpha (Col-Ialpha) mRNA expression was detected using RNase protection assays.
Serum alanine transaminase increased 8-fold above normal levels one day after BDL. Surprisingly, enzyme release was not reduced in rats receiving CoPP. Liver fibrosis was evaluated 3 wk after BDL and the sirius red-positive area was found to be increased to about 7.8%. However, in CoPP pretreated rats sirius red-positive areas were increased to about 11.7% after BDL. Collagen-Ialpha and TGF-beta mRNA increased significantly by BDL. Again, this effect was increased by HO-1 overexpression.
Hepatic fibrosis due to BDL is not reduced by the HO-1 inducer CoPP. In contrast, HO-1 overexpression increases liver injury in rats under conditions of experimental chronic cholestasis.</abstract><cop>United States</cop><pub>Department of Surgery, University of Osaka,Japan</pub><pmid>17659695</pmid><doi>10.3748/wjg.v13.i25.3478</doi><tpages>9</tpages><oa>free_for_read</oa></addata></record> |
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| identifier | ISSN: 1007-9327 |
| ispartof | World journal of gastroenterology : WJG, 2007-07, Vol.13 (25), p.3478-3486 |
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| subjects | Actins - analysis Alanine Transaminase - blood Animals Basic Research Bile Ducts Cholestasis - complications Cholestasis - enzymology Chronic Disease Heme Oxygenase-1 - physiology Immunohistochemistry Ligation Liver - enzymology Liver Cirrhosis - etiology Male Rats Rats, Sprague-Dawley RNA, Messenger - analysis Transforming Growth Factor beta1 - genetics Tumor Necrosis Factor-alpha - genetics |
| title | Heme oxygenase-1 overexpression increases liver injury after bile duct ligation in rats |
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