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Article: Antiinflammatory properties of IL-10 rescue small-for-size liver grafts

TitleAntiinflammatory properties of IL-10 rescue small-for-size liver grafts
Authors
Issue Date2007
PublisherJohn Wiley & Sons, Inc. The Journal's web site is located at http://www3.interscience.wiley.com/cgi-bin/jtoc/106570021
Citation
Liver Transplantation, 2007, v. 13 n. 4, p. 558-565 How to Cite?
Abstract
The present study aims to investigate the potential therapeutic role of interleukin-10 (IL-10) in small-for-size liver transplantation. A syngenic rat orthotopic liver transplantation model was performed using either whole or 40% liver volume of Lewis rats as grafts according to the experimental design. IL-10 was given to the 40% grafts right after reperfusion, and also at 24 and 48 hours after transplantation. When no treatment was given, less than 40% of the small-for-size grafts survived indefinitely, whereas IL-10 treatment could increase the long-term survival rate of the small-for-size grafts to 80%. The 40% grafts presented with extensive areas of necrosis and increased number of apoptotic cells at the early phases after reperfusion. In addition, upregulation of plasma protein carbonyl content (PCC) levels was also detected in the 40% graft group. IL-10 treatment suppressed the upregulation of allograft inflammatory factor-1 (AIF-1) on macrophages in the 40% grafts, and at the same time, decreased the levels of plasma PCC, and improved the histology and function of the 40% grafts. The expression of inducible nitric oxide synthase (iNOS), tumor necrosis factor (TNF)-α, and caspase 9 in the 40% grafts were upregulated after reperfusion, whereas the augmentation could be suppressed by the administration of IL-10. Finally, IL-10 culture could block AIF-1-mediated NO production and downregulate the expression of iNOS and TNF-α in a macrophage cell line. In conclusion, IL-10 rescued the small-for-size liver grafts by its antiinflammatory properties, through inhibition of AIF-1 mediated proinflammatory and proapoptotic activities of the macrophages during the early period after ischemia/reperfusion. © 2007 AASLD.
Persistent Identifierhttp://hdl.handle.net/10722/83752
ISSN
2013 Impact Factor: 3.793
ISI Accession Number ID
References

 

Author Affiliations
  1. The University of Hong Kong
  2. Faculty of Medicine
DC FieldValueLanguage
dc.contributor.authorYang, ZFen_HK
dc.contributor.authorHo, DWYen_HK
dc.contributor.authorNgai, Pen_HK
dc.contributor.authorLau, CKen_HK
dc.contributor.authorZhao, Yen_HK
dc.contributor.authorPoon, RTPen_HK
dc.contributor.authorFan, STen_HK
dc.date.accessioned2010-09-06T08:44:47Z-
dc.date.available2010-09-06T08:44:47Z-
dc.date.issued2007en_HK
dc.identifier.citationLiver Transplantation, 2007, v. 13 n. 4, p. 558-565en_HK
dc.identifier.issn1527-6465en_HK
dc.identifier.urihttp://hdl.handle.net/10722/83752-
dc.description.abstractThe present study aims to investigate the potential therapeutic role of interleukin-10 (IL-10) in small-for-size liver transplantation. A syngenic rat orthotopic liver transplantation model was performed using either whole or 40% liver volume of Lewis rats as grafts according to the experimental design. IL-10 was given to the 40% grafts right after reperfusion, and also at 24 and 48 hours after transplantation. When no treatment was given, less than 40% of the small-for-size grafts survived indefinitely, whereas IL-10 treatment could increase the long-term survival rate of the small-for-size grafts to 80%. The 40% grafts presented with extensive areas of necrosis and increased number of apoptotic cells at the early phases after reperfusion. In addition, upregulation of plasma protein carbonyl content (PCC) levels was also detected in the 40% graft group. IL-10 treatment suppressed the upregulation of allograft inflammatory factor-1 (AIF-1) on macrophages in the 40% grafts, and at the same time, decreased the levels of plasma PCC, and improved the histology and function of the 40% grafts. The expression of inducible nitric oxide synthase (iNOS), tumor necrosis factor (TNF)-α, and caspase 9 in the 40% grafts were upregulated after reperfusion, whereas the augmentation could be suppressed by the administration of IL-10. Finally, IL-10 culture could block AIF-1-mediated NO production and downregulate the expression of iNOS and TNF-α in a macrophage cell line. In conclusion, IL-10 rescued the small-for-size liver grafts by its antiinflammatory properties, through inhibition of AIF-1 mediated proinflammatory and proapoptotic activities of the macrophages during the early period after ischemia/reperfusion. © 2007 AASLD.en_HK
dc.languageengen_HK
dc.publisherJohn Wiley & Sons, Inc. The Journal's web site is located at http://www3.interscience.wiley.com/cgi-bin/jtoc/106570021en_HK
dc.relation.ispartofLiver Transplantationen_HK
dc.rightsLiver Transplantation. Copyright © John Wiley & Sons, Inc.en_HK
dc.titleAntiinflammatory properties of IL-10 rescue small-for-size liver graftsen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=1527-6465&volume=13&issue=4&spage=558&epage=565&date=2007&atitle=Antiinflammatory+properties+of+IL-10+rescue+small-for-size+liver+graftsen_HK
dc.identifier.emailPoon, RTP: poontp@hkucc.hku.hken_HK
dc.identifier.emailFan, ST: stfan@hku.hken_HK
dc.identifier.authorityPoon, RTP=rp00446en_HK
dc.identifier.authorityFan, ST=rp00355en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1002/lt.21094en_HK
dc.identifier.pmid17394154en_HK
dc.identifier.scopuseid_2-s2.0-34247235684en_HK
dc.identifier.hkuros126589en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-34247235684&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume13en_HK
dc.identifier.issue4en_HK
dc.identifier.spage558en_HK
dc.identifier.epage565en_HK
dc.identifier.isiWOS:000245596400015-
dc.publisher.placeUnited Statesen_HK
dc.identifier.scopusauthoridYang, ZF=14018809600en_HK
dc.identifier.scopusauthoridHo, DWY=7402971906en_HK
dc.identifier.scopusauthoridNgai, P=23477971900en_HK
dc.identifier.scopusauthoridLau, CK=7401968442en_HK
dc.identifier.scopusauthoridZhao, Y=7407402718en_HK
dc.identifier.scopusauthoridPoon, RTP=7103097223en_HK
dc.identifier.scopusauthoridFan, ST=7402678224en_HK

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