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Article: Epigallocatechin-3-gallate (EGCG) reduces liver inflammation, oxidative stress and fibrosis in carbon tetrachloride (CCl 4)-induced liver injury in mice

TitleEpigallocatechin-3-gallate (EGCG) reduces liver inflammation, oxidative stress and fibrosis in carbon tetrachloride (CCl 4)-induced liver injury in mice
Authors
KeywordsCarbon tetrachloride (CCl 4)
Epigallocatechin-3-gallate (EGCG)
Liver fibrosis
Liver inflammation
Oxidative stress
Issue Date2010
PublisherElsevier Ireland Ltd. The Journal's web site is located at http://www.elsevier.com/locate/toxicol
Citation
Toxicology, 2010, v. 273 n. 1-3, p. 45-52 How to Cite?
AbstractThe anti-inflammatory and antioxidant effects of epigallocatechin-3-gallate (EGCG) are considered important forces in attenuate liver injury and fibrosis. The aim of the study was to investigate the effect of EGCG on the expression of fibrogenic factors and whether EGCG attenuates the severity of oxidative stress and inflammatory response in chronic liver injury. Mice were administered with CCl 4 together with or without EGCG for 8 weeks (n=6-8 per group). Histopathological and biochemical analyses were carried out. The mRNA expression levels of TNF-α, COX-2, iNOS, α-smooth muscle actin (α-SMA), transforming growth factor (TGF-β 1), pro-collagen-I, matrix metalloproteinases (MMP-2, -9) and their inhibitors (TIMP-1, -2) were determined by RT-PCR. The collagen deposited in the liver was detected by Sirius Red staining. The formation of nitrotyrosine was measured as a marker of oxidative stress. The activity level of NF-κB and the expression level of C/EBP were also assessed. Chronic CCl 4 treatment caused liver injury, oxidative stress and nitrosative stress, and collagen accumulation in the liver. The expression levels of pro-inflammatory and pro-fibrotic mediators and the activity of NF-κB were increased. Treatment with EGCG significantly reduced liver injury, oxidative stress and the inflammatory response. EGCG also significantly reduced the formation of collagen in the liver, the expression of α-SMA and all of the assayed pro-fibrogenic markers except TIMP-2 and MMP-9. EGCG significantly attenuated the severity of CCl 4-induced liver injury and the progression of liver fibrosis. The protective effect of EGCG may in part be a consequence of the reduction in oxidative stress and the pro-inflammatory response. © 2010 Elsevier Ireland Ltd.
Persistent Identifierhttp://hdl.handle.net/10722/149744
ISSN
2015 Impact Factor: 3.817
2015 SCImago Journal Rankings: 1.335
ISI Accession Number ID
Funding AgencyGrant Number
Committee of Research and Conference Grants
University of Hong Kong, Hong Kong
Funding Information:

We would like to thank Miss. Carman Leung for her technical assistance in this project. This study was supported by a grant from the Committee of Research and Conference Grants, The University of Hong Kong, Hong Kong.

References

 

DC FieldValueLanguage
dc.contributor.authorTipoe, GLen_HK
dc.contributor.authorLeung, TMen_HK
dc.contributor.authorLiong, ECen_HK
dc.contributor.authorLau, TYHen_HK
dc.contributor.authorFung, MLen_HK
dc.contributor.authorNanji, AAen_HK
dc.date.accessioned2012-06-26T05:57:54Z-
dc.date.available2012-06-26T05:57:54Z-
dc.date.issued2010en_HK
dc.identifier.citationToxicology, 2010, v. 273 n. 1-3, p. 45-52en_HK
dc.identifier.issn0300-483Xen_HK
dc.identifier.urihttp://hdl.handle.net/10722/149744-
dc.description.abstractThe anti-inflammatory and antioxidant effects of epigallocatechin-3-gallate (EGCG) are considered important forces in attenuate liver injury and fibrosis. The aim of the study was to investigate the effect of EGCG on the expression of fibrogenic factors and whether EGCG attenuates the severity of oxidative stress and inflammatory response in chronic liver injury. Mice were administered with CCl 4 together with or without EGCG for 8 weeks (n=6-8 per group). Histopathological and biochemical analyses were carried out. The mRNA expression levels of TNF-α, COX-2, iNOS, α-smooth muscle actin (α-SMA), transforming growth factor (TGF-β 1), pro-collagen-I, matrix metalloproteinases (MMP-2, -9) and their inhibitors (TIMP-1, -2) were determined by RT-PCR. The collagen deposited in the liver was detected by Sirius Red staining. The formation of nitrotyrosine was measured as a marker of oxidative stress. The activity level of NF-κB and the expression level of C/EBP were also assessed. Chronic CCl 4 treatment caused liver injury, oxidative stress and nitrosative stress, and collagen accumulation in the liver. The expression levels of pro-inflammatory and pro-fibrotic mediators and the activity of NF-κB were increased. Treatment with EGCG significantly reduced liver injury, oxidative stress and the inflammatory response. EGCG also significantly reduced the formation of collagen in the liver, the expression of α-SMA and all of the assayed pro-fibrogenic markers except TIMP-2 and MMP-9. EGCG significantly attenuated the severity of CCl 4-induced liver injury and the progression of liver fibrosis. The protective effect of EGCG may in part be a consequence of the reduction in oxidative stress and the pro-inflammatory response. © 2010 Elsevier Ireland Ltd.en_HK
dc.languageengen_US
dc.publisherElsevier Ireland Ltd. The Journal's web site is located at http://www.elsevier.com/locate/toxicolen_HK
dc.relation.ispartofToxicologyen_HK
dc.subjectCarbon tetrachloride (CCl 4)en_HK
dc.subjectEpigallocatechin-3-gallate (EGCG)en_HK
dc.subjectLiver fibrosisen_HK
dc.subjectLiver inflammationen_HK
dc.subjectOxidative stressen_HK
dc.subject.meshActins - Metabolismen_US
dc.subject.meshAnimalsen_US
dc.subject.meshAnti-Inflammatory Agents - Therapeutic Useen_US
dc.subject.meshCarbon Tetrachlorideen_US
dc.subject.meshCatechin - Analogs & Derivatives - Therapeutic Useen_US
dc.subject.meshCollagen Type I - Metabolismen_US
dc.subject.meshCyclooxygenase 2 Inhibitors - Metabolismen_US
dc.subject.meshDrug-Induced Liver Injury - Drug Therapy - Metabolismen_US
dc.subject.meshLiver Cirrhosis - Drug Therapy - Metabolismen_US
dc.subject.meshMaleen_US
dc.subject.meshMatrix Metalloproteinases - Metabolismen_US
dc.subject.meshMiceen_US
dc.subject.meshMice, Inbred C57blen_US
dc.subject.meshNitric Oxide Synthase Type Ii - Metabolismen_US
dc.subject.meshOxidative Stress - Drug Effectsen_US
dc.subject.meshTissue Inhibitor Of Metalloproteinases - Metabolismen_US
dc.subject.meshTransforming Growth Factor Beta1 - Metabolismen_US
dc.subject.meshTumor Necrosis Factor-Alpha - Metabolismen_US
dc.subject.meshTyrosine - Analogs & Derivatives - Metabolismen_US
dc.titleEpigallocatechin-3-gallate (EGCG) reduces liver inflammation, oxidative stress and fibrosis in carbon tetrachloride (CCl 4)-induced liver injury in miceen_HK
dc.typeArticleen_HK
dc.identifier.emailTipoe, GL: tgeorge@hkucc.hku.hken_HK
dc.identifier.emailFung, ML: fungml@hkucc.hku.hken_HK
dc.identifier.authorityTipoe, GL=rp00371en_HK
dc.identifier.authorityFung, ML=rp00433en_HK
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.1016/j.tox.2010.04.014en_HK
dc.identifier.pmid20438794-
dc.identifier.scopuseid_2-s2.0-77953279213en_HK
dc.identifier.hkuros170681-
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-77953279213&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume273en_HK
dc.identifier.issue1-3en_HK
dc.identifier.spage45en_HK
dc.identifier.epage52en_HK
dc.identifier.eissn1879-3185-
dc.identifier.isiWOS:000279426900006-
dc.publisher.placeIrelanden_HK
dc.identifier.scopusauthoridTipoe, GL=7003550610en_HK
dc.identifier.scopusauthoridLeung, TM=7202110149en_HK
dc.identifier.scopusauthoridLiong, EC=6602732210en_HK
dc.identifier.scopusauthoridLau, TYH=26323763000en_HK
dc.identifier.scopusauthoridFung, ML=7101955092en_HK
dc.identifier.scopusauthoridNanji, AA=35885060300en_HK
dc.identifier.citeulike7149788-

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