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Article: Senkyunolides reduce hydrogen peroxide-induced oxidative damage in human liver HepG2 cells via induction of heme oxygenase-1

TitleSenkyunolides reduce hydrogen peroxide-induced oxidative damage in human liver HepG2 cells via induction of heme oxygenase-1
Authors
Qi, HSiu, SOChen, YHan, YChu, IKTong, YLau, ASYRong, J
KeywordsAntioxidation
Bioactivity-guided fractionation
Cytoprotection
Heme oxygenase 1
Rhizoma Chuanxiong
Issue Date2010
PublisherElsevier Ireland Ltd. The Journal's web site is located at http://www.elsevier.com/locate/chembioint
Citation
Chemico-Biological Interactions, 2010, v. 183 n. 3, p. 380-389 How to Cite?
DOI: http://dx.doi.org/10.1016/j.cbi.2009.11.029
AbstractRhizoma Chuanxiong is widely used as folk medicine to treat the diseases caused by oxidative stress and inflammation. To delineate the underlying molecular mechanisms, we recently found that Rhizoma Chuanxiong extract significantly induced heme oxygenase-1 (HO-1), an enzyme that degrades intracellular heme into three bioactive products: biliverdin, carbon monoxide and free iron. The anti-inflammatory, antiapoptotic and antiproliferative actions of these products highlight HO-1 as a key endogenous antioxidant and cytoprotective gene. This study was designed to further characterize HO-1 induction of Rhizoma Chuanxiong through bioactivity-guided fractionation. All isolated fractions were assayed for HO-1 induction in human HepG2 cell line at mRNA and protein levels. Based on chromatographic profiling, nuclear magnetic resonance (NMR) and mass spectrometric analysis, the active compounds were identified as senkyunolide-H and its stereoisomer senkyunolide-I. Both senkyunolide isomers inhibited the formation of reactive oxygen species and lipid peroxidation and enhanced the cellular resistance to hydrogen peroxide-induced oxidative damage. Notably, heme oxygenase inhibitor tin protoporphyrin IX (SnPP) significantly suppressed the antioxidant activity of senkyunolide stereoisomers. Thus, this study demonstrated that senkyunolide-H and -I attenuated oxidative damage via activation of HO-1 pathway. © 2009 Elsevier Ireland Ltd. All rights reserved.
Persistent Identifierhttp://hdl.handle.net/10722/127615
ISSN
0009-2797
2023 Impact Factor: 4.7
2023 SCImago Journal Rankings: 0.946
ISI Accession Number ID
WOS:000274828700007
Funding AgencyGrant Number
Research Grants Council of Hong KongHKU774307 M
Funding Information:

This work was supported by a General Research Fund (GRF) grant (HKU774307 M) from the Research Grants Council of Hong Kong (to J.R.). Authors acknowledge Professor Qinglin Zhang (Beijing Institute of Radiation Medicine) for performing 1HNMR analysis.

References
References in Scopus

 

DC FieldValueLanguage
dc.contributor.authorQi, Hen_HK
dc.contributor.authorSiu, SOen_HK
dc.contributor.authorChen, Yen_HK
dc.contributor.authorHan, Yen_HK
dc.contributor.authorChu, IKen_HK
dc.contributor.authorTong, Yen_HK
dc.contributor.authorLau, ASYen_HK
dc.contributor.authorRong, Jen_HK
dc.date.accessioned2010-10-31T13:35:47Z-
dc.date.available2010-10-31T13:35:47Z-
dc.date.issued2010en_HK
dc.identifier.citationChemico-Biological Interactions, 2010, v. 183 n. 3, p. 380-389en_HK
dc.identifier.issn0009-2797en_HK
dc.identifier.urihttp://hdl.handle.net/10722/127615-
dc.description.abstractRhizoma Chuanxiong is widely used as folk medicine to treat the diseases caused by oxidative stress and inflammation. To delineate the underlying molecular mechanisms, we recently found that Rhizoma Chuanxiong extract significantly induced heme oxygenase-1 (HO-1), an enzyme that degrades intracellular heme into three bioactive products: biliverdin, carbon monoxide and free iron. The anti-inflammatory, antiapoptotic and antiproliferative actions of these products highlight HO-1 as a key endogenous antioxidant and cytoprotective gene. This study was designed to further characterize HO-1 induction of Rhizoma Chuanxiong through bioactivity-guided fractionation. All isolated fractions were assayed for HO-1 induction in human HepG2 cell line at mRNA and protein levels. Based on chromatographic profiling, nuclear magnetic resonance (NMR) and mass spectrometric analysis, the active compounds were identified as senkyunolide-H and its stereoisomer senkyunolide-I. Both senkyunolide isomers inhibited the formation of reactive oxygen species and lipid peroxidation and enhanced the cellular resistance to hydrogen peroxide-induced oxidative damage. Notably, heme oxygenase inhibitor tin protoporphyrin IX (SnPP) significantly suppressed the antioxidant activity of senkyunolide stereoisomers. Thus, this study demonstrated that senkyunolide-H and -I attenuated oxidative damage via activation of HO-1 pathway. © 2009 Elsevier Ireland Ltd. All rights reserved.en_HK
dc.languageengen_HK
dc.publisherElsevier Ireland Ltd. The Journal's web site is located at http://www.elsevier.com/locate/chembiointen_HK
dc.relation.ispartofChemico-Biological Interactionsen_HK
dc.subjectAntioxidationen_HK
dc.subjectBioactivity-guided fractionationen_HK
dc.subjectCytoprotectionen_HK
dc.subjectHeme oxygenase 1en_HK
dc.subjectRhizoma Chuanxiongen_HK
dc.subject.meshBenzofurans - pharmacology-
dc.subject.meshEnzyme Inhibitors - pharmacology-
dc.subject.meshHeme Oxygenase-1 - genetics - metabolism-
dc.subject.meshHydrogen Peroxide - toxicity-
dc.subject.meshOxidative Stress - drug effects-
dc.titleSenkyunolides reduce hydrogen peroxide-induced oxidative damage in human liver HepG2 cells via induction of heme oxygenase-1en_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0009-2797&volume=183&issue=3&spage=380&epage=389&date=2010&atitle=Senkyunolides+reduce+hydrogen+peroxide-induced+oxidative+damage+in+human+liver+HepG2+cells+via+induction+of+heme+oxygenase-1-
dc.identifier.emailChen, Y: ychenc@hku.hken_HK
dc.identifier.emailChu, IK: ivankchu@hku.hken_HK
dc.identifier.emailTong, Y: tongyao@hku.hken_HK
dc.identifier.emailLau, ASY: asylau@hku.hken_HK
dc.identifier.emailRong, J: jrong@hku.hken_HK
dc.identifier.authorityChen, Y=rp01318en_HK
dc.identifier.authorityChu, IK=rp00683en_HK
dc.identifier.authorityTong, Y=rp00509en_HK
dc.identifier.authorityLau, ASY=rp00474en_HK
dc.identifier.authorityRong, J=rp00515en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1016/j.cbi.2009.11.029en_HK
dc.identifier.pmid19961840-
dc.identifier.scopuseid_2-s2.0-74149085006en_HK
dc.identifier.hkuros197189en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-74149085006&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume183en_HK
dc.identifier.issue3en_HK
dc.identifier.spage380en_HK
dc.identifier.epage389en_HK
dc.identifier.eissn1872-7786-
dc.identifier.isiWOS:000274828700007-
dc.publisher.placeIrelanden_HK
dc.identifier.scopusauthoridQi, H=35367105300en_HK
dc.identifier.scopusauthoridSiu, SO=8603087200en_HK
dc.identifier.scopusauthoridChen, Y=36463185300en_HK
dc.identifier.scopusauthoridHan, Y=8527680500en_HK
dc.identifier.scopusauthoridChu, IK=7103327484en_HK
dc.identifier.scopusauthoridTong, Y=9045384000en_HK
dc.identifier.scopusauthoridLau, ASY=7202626202en_HK
dc.identifier.scopusauthoridRong, J=7005980047en_HK
dc.identifier.citeulike6409491-
dc.identifier.issnl0009-2797-

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