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Article: S-allylmercaptocysteine reduces carbon tetrachloride-induced hepatic oxidative stress and necroinflammation via nuclear factor kappa B-dependent pathways in mice

TitleS-allylmercaptocysteine reduces carbon tetrachloride-induced hepatic oxidative stress and necroinflammation via nuclear factor kappa B-dependent pathways in mice
Authors
KeywordsCarbon tetrachloride
Liver injury
Necroinflammation
Nuclear factor κB
Oxidative stress
S-allylmercaptocysteine
Issue Date2012
PublisherDr Dietrich Steinkopff Verlag. The Journal's web site is located at http://link.springer.de/link/service/journals/00394/index.htm
Citation
European Journal Of Nutrition, 2012, v. 51 n. 3, p. 323-333 How to Cite?
AbstractPurpose: To study the protective effects and underlying molecular mechanisms of SAMC on carbon tetrachloride (CCl 4)-induced acute hepatotoxicity in the mouse model. Methods: Mice were intraperitoneally injected with CCl 4 (50 μl/kg; single dose) to induce acute hepatotoxicity with or without a 2-h pre-treatment of SAMC intraperitoneal injection (200 mg/kg; single dose). After 8 h, the blood serum and liver samples of mice were collected and subjected to measurements of histological and molecular parameters of hepatotoxicity. Results: SAMC reduced CCl 4-triggered cellular necrosis and inflammation in the liver under histological analysis. Since co-treatment of SAMC and CCl 4 enhanced the expressions of antioxidant enzymes, reduced the nitric oxide (NO)-dependent oxidative stress, and inhibited lipid peroxidation induced by CCl 4. SAMC played an essential antioxidative role during CCl 4-induced hepatotoxicity. Administration of SAMC also ameliorated hepatic inflammation induced by CCl 4 via inhibiting the activity of NF-κB subunits p50 and p65, thus reducing the expressions of pro-inflammatory cytokines, mediators, and chemo-kines, as well as promoting pro-regenerative factors at both transcriptional and translational levels. Conclusions: Our results indicate that SAMC mitigates cellular damage, oxidative stress, and inflammation in CCl4-induced acute hepatotoxicity mouse model through regulation of NF-κB. Garlic or garlic derivatives may therefore be a potential food supplement in the prevention of liver damage. © The Author(s) 2011. This article is published with open access at Springerlink.com.
Persistent Identifierhttp://hdl.handle.net/10722/144921
ISSN
2015 Impact Factor: 3.239
2015 SCImago Journal Rankings: 1.337
PubMed Central ID
ISI Accession Number ID
Funding AgencyGrant Number
University Research Committee
The University of Hong Kong
University Grant Council, Hong Kong SAR
Funding Information:

We would like to thank Ms. Carman Leung for her technical help in this project. This study is partly supported by Small Project Funding, University Research Committee, The University of Hong Kong and General Research Fund, University Grant Council, Hong Kong SAR.

References

 

DC FieldValueLanguage
dc.contributor.authorXiao, Jen_HK
dc.contributor.authorLiong, ECen_HK
dc.contributor.authorLing, MTen_HK
dc.contributor.authorChing, YPen_HK
dc.contributor.authorFung, MLen_HK
dc.contributor.authorTipoe, GLen_HK
dc.date.accessioned2012-02-21T05:43:02Z-
dc.date.available2012-02-21T05:43:02Z-
dc.date.issued2012en_HK
dc.identifier.citationEuropean Journal Of Nutrition, 2012, v. 51 n. 3, p. 323-333en_HK
dc.identifier.issn1436-6207en_HK
dc.identifier.urihttp://hdl.handle.net/10722/144921-
dc.description.abstractPurpose: To study the protective effects and underlying molecular mechanisms of SAMC on carbon tetrachloride (CCl 4)-induced acute hepatotoxicity in the mouse model. Methods: Mice were intraperitoneally injected with CCl 4 (50 μl/kg; single dose) to induce acute hepatotoxicity with or without a 2-h pre-treatment of SAMC intraperitoneal injection (200 mg/kg; single dose). After 8 h, the blood serum and liver samples of mice were collected and subjected to measurements of histological and molecular parameters of hepatotoxicity. Results: SAMC reduced CCl 4-triggered cellular necrosis and inflammation in the liver under histological analysis. Since co-treatment of SAMC and CCl 4 enhanced the expressions of antioxidant enzymes, reduced the nitric oxide (NO)-dependent oxidative stress, and inhibited lipid peroxidation induced by CCl 4. SAMC played an essential antioxidative role during CCl 4-induced hepatotoxicity. Administration of SAMC also ameliorated hepatic inflammation induced by CCl 4 via inhibiting the activity of NF-κB subunits p50 and p65, thus reducing the expressions of pro-inflammatory cytokines, mediators, and chemo-kines, as well as promoting pro-regenerative factors at both transcriptional and translational levels. Conclusions: Our results indicate that SAMC mitigates cellular damage, oxidative stress, and inflammation in CCl4-induced acute hepatotoxicity mouse model through regulation of NF-κB. Garlic or garlic derivatives may therefore be a potential food supplement in the prevention of liver damage. © The Author(s) 2011. This article is published with open access at Springerlink.com.en_HK
dc.languageengen_US
dc.publisherDr Dietrich Steinkopff Verlag. The Journal's web site is located at http://link.springer.de/link/service/journals/00394/index.htmen_HK
dc.relation.ispartofEuropean Journal of Nutritionen_HK
dc.rightsThe Author(s)en_US
dc.rightsCreative Commons: Attribution 3.0 Hong Kong Licenseen_US
dc.subjectCarbon tetrachlorideen_HK
dc.subjectLiver injuryen_HK
dc.subjectNecroinflammationen_HK
dc.subjectNuclear factor κBen_HK
dc.subjectOxidative stressen_HK
dc.subjectS-allylmercaptocysteineen_HK
dc.titleS-allylmercaptocysteine reduces carbon tetrachloride-induced hepatic oxidative stress and necroinflammation via nuclear factor kappa B-dependent pathways in miceen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4551/resserv?sid=springerlink&genre=article&atitle=S-allylmercaptocysteine reduces carbon tetrachloride-induced hepatic oxidative stress and necroinflammation via nuclear factor kappa B-dependent pathways in mice&title=European Journal of Nutrition&issn=14366207&date=2011-06-17& spage=1&authors=Jia Xiao, Emily C. Liong, Ming-Tat Ling, <i>et al.</i>en_US
dc.identifier.emailLing, MT: patling@hkucc.hku.hken_HK
dc.identifier.emailChing, YP: ypching@hku.hken_HK
dc.identifier.emailFung, ML: fungml@hkucc.hku.hken_HK
dc.identifier.emailTipoe, GL: tgeorge@hkucc.hku.hken_HK
dc.identifier.emailLiong, EC: eclionga@hkucc.hku.hk-
dc.identifier.authorityLing, MT=rp00449en_HK
dc.identifier.authorityChing, YP=rp00469en_HK
dc.identifier.authorityFung, ML=rp00433en_HK
dc.identifier.authorityTipoe, GL=rp00371en_HK
dc.description.naturepublished_or_final_versionen_US
dc.identifier.doi10.1007/s00394-011-0217-0en_HK
dc.identifier.pmid21681437-
dc.identifier.pmcidPMC3313023-
dc.identifier.scopuseid_2-s2.0-84860671363en_HK
dc.identifier.hkuros200045-
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-84860671363&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume51en_HK
dc.identifier.issue3en_HK
dc.identifier.spage323en_HK
dc.identifier.epage333en_HK
dc.identifier.eissn1436-6215en_US
dc.identifier.isiWOS:000302231800006-
dc.publisher.placeGermanyen_HK
dc.description.otherSpringer Open Choice, 21 Feb 2012en_US
dc.identifier.scopusauthoridXiao, J=40462781100en_HK
dc.identifier.scopusauthoridLiong, EC=6602732210en_HK
dc.identifier.scopusauthoridLing, MT=7102229780en_HK
dc.identifier.scopusauthoridChing, YP=7005431277en_HK
dc.identifier.scopusauthoridFung, ML=7101955092en_HK
dc.identifier.scopusauthoridTipoe, GL=7003550610en_HK
dc.identifier.citeulike9444489-

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