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Article: Therapeutic potential of cardiotrophin 1 in fulminant hepatic failure: Dual roles in antiapoptosis and cell repair

TitleTherapeutic potential of cardiotrophin 1 in fulminant hepatic failure: Dual roles in antiapoptosis and cell repair
Authors
Issue Date2006
PublisherAmerican Medical Association. The Journal's web site is located at http://www.archsurg.com
Citation
Archives Of Surgery, 2006, v. 141 n. 11, p. 1077-1084 How to Cite?
AbstractHypothesis: Administration of cardiotrophin 1 (CT-1) can treat experimental fulminant hepatic failure (FHF). Design: Rat model with FHF induced by D-galactosamine (D-gal). Setting: Fulminant hepatic failure is a rapidly progressive disease that lacks effective nonsurgical treatment. Cardiotrophin 1 is a member of the interleukin 6 family that can protect cells from damage in some animal disease models. Animals: A rat model of FHF was induced by an intraperitoneal injection of D-gal (1.4 g/kg of body weight). Cardiotrophin 1 was administered at different time points after D-gal injection. Results: Administration of CT-1 at 12 and 18 hours had a survival rate of 80% (12/15) and 70% (7/10), respectively, which was significantly higher than that of nontreatment (28% [5/18]). In addition, improvement of liver histologic findings, shortening of activated clotting time, and decrease in serum levels of total bilirubin and alanine aminotransferase were detected with CT-1 treatment. Administration of CT-1 decreased apoptotic cells and increased Ki-67 cells in the liver tissues. In vitro, CT-1 administration significantly decreased apoptotic cells and sequentially down-regulated the expression of proapoptotic molecules and up-regulated the expression of antiapoptotic molecules at different culture periods. D-galactosamine culture induced morphologic damage in a hepatocyte cell line, which was greatly improved by CT-1 administration. In addition, CT-1-treated cells demonstrated increased expression of glycoprotein 130 and upregulation of cyclin D1 and heat shock protein 90. Conclusion: Cardiotrophin 1 may improve the outcome of D-gal-induced FHF through its effects on antiapoptosis and cell repair. ©2006 American Medical Association. All rights reserved.
Persistent Identifierhttp://hdl.handle.net/10722/83094
ISSN
2014 Impact Factor: 4.926
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorHo, DWen_HK
dc.contributor.authorZhen, FYen_HK
dc.contributor.authorChi, KLen_HK
dc.contributor.authorKa, HTen_HK
dc.contributor.authorTo, JYen_HK
dc.contributor.authorPoon, RTen_HK
dc.contributor.authorSheung, TFen_HK
dc.date.accessioned2010-09-06T08:36:56Z-
dc.date.available2010-09-06T08:36:56Z-
dc.date.issued2006en_HK
dc.identifier.citationArchives Of Surgery, 2006, v. 141 n. 11, p. 1077-1084en_HK
dc.identifier.issn0004-0010en_HK
dc.identifier.urihttp://hdl.handle.net/10722/83094-
dc.description.abstractHypothesis: Administration of cardiotrophin 1 (CT-1) can treat experimental fulminant hepatic failure (FHF). Design: Rat model with FHF induced by D-galactosamine (D-gal). Setting: Fulminant hepatic failure is a rapidly progressive disease that lacks effective nonsurgical treatment. Cardiotrophin 1 is a member of the interleukin 6 family that can protect cells from damage in some animal disease models. Animals: A rat model of FHF was induced by an intraperitoneal injection of D-gal (1.4 g/kg of body weight). Cardiotrophin 1 was administered at different time points after D-gal injection. Results: Administration of CT-1 at 12 and 18 hours had a survival rate of 80% (12/15) and 70% (7/10), respectively, which was significantly higher than that of nontreatment (28% [5/18]). In addition, improvement of liver histologic findings, shortening of activated clotting time, and decrease in serum levels of total bilirubin and alanine aminotransferase were detected with CT-1 treatment. Administration of CT-1 decreased apoptotic cells and increased Ki-67 cells in the liver tissues. In vitro, CT-1 administration significantly decreased apoptotic cells and sequentially down-regulated the expression of proapoptotic molecules and up-regulated the expression of antiapoptotic molecules at different culture periods. D-galactosamine culture induced morphologic damage in a hepatocyte cell line, which was greatly improved by CT-1 administration. In addition, CT-1-treated cells demonstrated increased expression of glycoprotein 130 and upregulation of cyclin D1 and heat shock protein 90. Conclusion: Cardiotrophin 1 may improve the outcome of D-gal-induced FHF through its effects on antiapoptosis and cell repair. ©2006 American Medical Association. All rights reserved.en_HK
dc.languageengen_HK
dc.publisherAmerican Medical Association. The Journal's web site is located at http://www.archsurg.comen_HK
dc.relation.ispartofArchives of Surgeryen_HK
dc.titleTherapeutic potential of cardiotrophin 1 in fulminant hepatic failure: Dual roles in antiapoptosis and cell repairen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0004-0010&volume=141&issue=11&spage=1077&epage=1084&date=2006&atitle=Therapeutic+potential+of+cardiotrophin-1+in+fulminant+hepatic+failure:+dual+roles+in+antiapoptosis+and+cell+repairen_HK
dc.identifier.emailPoon, RT: poontp@hkucc.hku.hken_HK
dc.identifier.authorityPoon, RT=rp00446en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1001/archsurg.141.11.1077en_HK
dc.identifier.pmid17116800-
dc.identifier.scopuseid_2-s2.0-33751241137en_HK
dc.identifier.hkuros125006en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-33751241137&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume141en_HK
dc.identifier.issue11en_HK
dc.identifier.spage1077en_HK
dc.identifier.epage1084en_HK
dc.identifier.isiWOS:000241918700005-
dc.publisher.placeUnited Statesen_HK
dc.identifier.scopusauthoridHo, DW=7402971906en_HK
dc.identifier.scopusauthoridZhen, FY=14018809600en_HK
dc.identifier.scopusauthoridChi, KL=15070609500en_HK
dc.identifier.scopusauthoridKa, HT=15070828800en_HK
dc.identifier.scopusauthoridTo, JY=6603618643en_HK
dc.identifier.scopusauthoridPoon, RT=7103097223en_HK
dc.identifier.scopusauthoridSheung, TF=6506234707en_HK

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