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Conference Paper: Green tea polyphenols (GTPS) reduced fibrogenesis in non-alcoholic fatty liver disease in rats

TitleGreen tea polyphenols (GTPS) reduced fibrogenesis in non-alcoholic fatty liver disease in rats
Authors
Issue Date2008
PublisherJohn Wiley & Sons, Inc. The Journal's web site is located at http://www.hepatology.org/
Citation
The 59th Annual Meeting of the American Association for the Study of Liver Diseases, San Francisco,, CA, 31 October-4 November 2008. In Hepatology, 2008, v. 48 n. S1, p. 841A Abstract no.1195 How to Cite?
AbstractBackground: Attention has been focused on the use of supple-mentary phytochemicals in the treatment of non-alcoholic fattyliver disease (NAFLD). Objective: We investigated whetherEGCG could modulate expression of profibrogenic markers inNAFLD. Experimental Design: We fed an unsaturated fat diet(30% fish oil) to female Sprague-Dawley rats (180-200g), con-sumed ad libitum for 8 weeks (NAFLD; n = 8). Control animals(CF; n = 8) were fed an isocaloric diet with commercial ratchow. To evaluate the effect of EGCG on NAFLD, rats in theNAFLD group was injected with EGCG intraperitoneally[50mg/kg] three times per week. The CF group received thevehicle. At killing, blood and liver samples were collected forserum alanine aminotransferase (ALT), histology and molecularanalysis. Each histological sample was evaluated for fatty liver(graded from 0-4+), necrosis (number of necrotic foci(no./mm2) and inflammation (cells per mm2). The amount ofcollagen formation was estimated using Sirius Red staining.Reverse transcription polymerase chain reaction (RT-PCR) wascarried out for TGF-β1, procollagen-I (Pro-col-I), tissue inhibitorsof metalloproteinases (TIMP-1, TIMP-2) matrix metalloproteinase(MMP-2). Zymography determined the enzyme activity of MMP-2. Electrophoretic mobility shift assay was performed fornuclear factor-kappa B (NF-kB) activity. Results: NAFLD rats hada significantly higher serum ALT level, fatty liver, necrosis,inflammation and amount of collagen formation (Sirius Redstaining) when compared with the CF rats (p< 0.05). ThemRNA levels of the profibrotic factors, TGF-β1, Pro-col-I, TIMP-1, TIMP-2 and MMP-2 were elevated in the NAFLD group (p<0.05). The MMP-2 enzyme and NF-kB activity were alsoincreased in the NAFLD rats (p<0.01). Treatment with EGCGsignificantly reduced the severity of pathological changeswhich include fatty change, necrosis and inflammation, fibrosis(Sirius Red) and down-regulated expression of TGF-β1, Pro-col-I, TIMP-1, TIMP-2 and MMP-2. Treatment with EGCG also sig-nificantly decreased the MMP-2 enzyme and NF-kB activity.Conclusion: EGCG decreased the degree of hepatic fibrosisand profibrogenic markers in rats fed with fish and dextrose.We proposed that the therapeutic effect of GTPs in NAFLD maybe mediated through down-regulation of profibrogenic factorsand its use can be considered as adjuvant therapy in fiborgenicliver disease.
Persistent Identifierhttp://hdl.handle.net/10722/61393
ISSN
2015 Impact Factor: 11.711
2015 SCImago Journal Rankings: 4.752

 

DC FieldValueLanguage
dc.contributor.authorTipoe, GL-
dc.contributor.authorHo, CT-
dc.contributor.authorLiong, EC-
dc.contributor.authorLeung, TM-
dc.contributor.authorLau, TYH-
dc.contributor.authorFung, ML-
dc.contributor.authorNanji, AA-
dc.date.accessioned2010-07-13T03:38:46Z-
dc.date.available2010-07-13T03:38:46Z-
dc.date.issued2008-
dc.identifier.citationThe 59th Annual Meeting of the American Association for the Study of Liver Diseases, San Francisco,, CA, 31 October-4 November 2008. In Hepatology, 2008, v. 48 n. S1, p. 841A Abstract no.1195-
dc.identifier.issn0270-9139-
dc.identifier.urihttp://hdl.handle.net/10722/61393-
dc.description.abstractBackground: Attention has been focused on the use of supple-mentary phytochemicals in the treatment of non-alcoholic fattyliver disease (NAFLD). Objective: We investigated whetherEGCG could modulate expression of profibrogenic markers inNAFLD. Experimental Design: We fed an unsaturated fat diet(30% fish oil) to female Sprague-Dawley rats (180-200g), con-sumed ad libitum for 8 weeks (NAFLD; n = 8). Control animals(CF; n = 8) were fed an isocaloric diet with commercial ratchow. To evaluate the effect of EGCG on NAFLD, rats in theNAFLD group was injected with EGCG intraperitoneally[50mg/kg] three times per week. The CF group received thevehicle. At killing, blood and liver samples were collected forserum alanine aminotransferase (ALT), histology and molecularanalysis. Each histological sample was evaluated for fatty liver(graded from 0-4+), necrosis (number of necrotic foci(no./mm2) and inflammation (cells per mm2). The amount ofcollagen formation was estimated using Sirius Red staining.Reverse transcription polymerase chain reaction (RT-PCR) wascarried out for TGF-β1, procollagen-I (Pro-col-I), tissue inhibitorsof metalloproteinases (TIMP-1, TIMP-2) matrix metalloproteinase(MMP-2). Zymography determined the enzyme activity of MMP-2. Electrophoretic mobility shift assay was performed fornuclear factor-kappa B (NF-kB) activity. Results: NAFLD rats hada significantly higher serum ALT level, fatty liver, necrosis,inflammation and amount of collagen formation (Sirius Redstaining) when compared with the CF rats (p< 0.05). ThemRNA levels of the profibrotic factors, TGF-β1, Pro-col-I, TIMP-1, TIMP-2 and MMP-2 were elevated in the NAFLD group (p<0.05). The MMP-2 enzyme and NF-kB activity were alsoincreased in the NAFLD rats (p<0.01). Treatment with EGCGsignificantly reduced the severity of pathological changeswhich include fatty change, necrosis and inflammation, fibrosis(Sirius Red) and down-regulated expression of TGF-β1, Pro-col-I, TIMP-1, TIMP-2 and MMP-2. Treatment with EGCG also sig-nificantly decreased the MMP-2 enzyme and NF-kB activity.Conclusion: EGCG decreased the degree of hepatic fibrosisand profibrogenic markers in rats fed with fish and dextrose.We proposed that the therapeutic effect of GTPs in NAFLD maybe mediated through down-regulation of profibrogenic factorsand its use can be considered as adjuvant therapy in fiborgenicliver disease.-
dc.languageeng-
dc.publisherJohn Wiley & Sons, Inc. The Journal's web site is located at http://www.hepatology.org/-
dc.relation.ispartofHepatology-
dc.rightsHepatology. Copyright © John Wiley & Sons, Inc.-
dc.rightsSpecial Statement for Preprint only Before publication: 'This is a preprint of an article accepted for publication in [The Journal of Pathology] Copyright © ([year]) ([Pathological Society of Great Britain and Ireland])'. After publication: the preprint notice should be amended to follows: 'This is a preprint of an article published in [include the complete citation information for the final version of the Contribution as published in the print edition of the Journal]' For Cochrane Library/ Cochrane Database of Systematic Reviews, add statement & acknowledgement : ‘This review is published as a Cochrane Review in the Cochrane Database of Systematic Reviews 20XX, Issue X. Cochrane Reviews are regularly updated as new evidence emerges and in response to comments and criticisms, and the Cochrane Database of Systematic Reviews should be consulted for the most recent version of the Review.’ Please include reference to the Review and hyperlink to the original version using the following format e.g. Authors. Title of Review. Cochrane Database of Systematic Reviews 20XX, Issue #. Art. No.: CD00XXXX. DOI: 10.1002/14651858.CD00XXXX (insert persistent link to the article by using the URL: http://dx.doi.org/10.1002/14651858.CD00XXXX) (This statement should refer to the most recent issue of the Cochrane Database of Systematic Reviews in which the Review published.)-
dc.titleGreen tea polyphenols (GTPS) reduced fibrogenesis in non-alcoholic fatty liver disease in rats-
dc.typeConference_Paper-
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0270-9139&volume=48&issue=4&spage=841A 1195&epage=&date=2008&atitle=Green+tea+polyphenols+(GTPS)+reduced+fibrogenesis+in+non-alcoholic+fatty+liver+disease+in+ratsen_HK
dc.identifier.emailTipoe, GL: tgeorge@hkucc.hku.hk-
dc.identifier.emailLiong, EC: eclionga@HKUCC.hku.hk-
dc.identifier.emailLeung, TM: leungtm@hkucc.hku.hk-
dc.identifier.emailFung, ML: fungml@hkucc.hku.hk-
dc.identifier.authorityTipoe, GL=rp00371-
dc.identifier.authorityFung, ML=rp00433-
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1002/hep.22645-
dc.identifier.hkuros160575-
dc.identifier.volume48-
dc.identifier.issueS1-
dc.identifier.spage841A Abstract no.1195-
dc.identifier.epage841A Abstract no.1195-
dc.publisher.placeUnited States-

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