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Article: Chinonin, a novel drug against cardiomyocyte apoptosis induced by hypoxia and reoxygenation

TitleChinonin, a novel drug against cardiomyocyte apoptosis induced by hypoxia and reoxygenation
Authors
Issue Date2000
PublisherElsevier BV. The Journal's web site is located at http://www.elsevier.com/locate/bbadis
Citation
Biochimica Et Biophysica Acta - Molecular Basis Of Disease, 2000, v. 1500 n. 2, p. 217-226 How to Cite?
AbstractThe inhibitory effects of Chinonin, a natural antioxidant extracted from a Chinese medicine, on apoptotic and necrotic cell death of cardiomyocytes in hypoxia-reoxygenation process were observed in this study. The possible mechanisms of Chinonin on scavenging reactive oxygen species and regulating apoptotic related genes bcl-2 and p53 were also investigated. Neonatal rat cardiomyocytes were subjected to 24-h hypoxia and 4-h reoxygenation. Cell death was evaluated by DNA electrophoresis on agarose gel, cell death ELISA and annexin-V-FLUOS/propidium iodide (PI) double staining cytometry. Hypoxia caused the increase of apoptotic rates and the release of lactate dehydrogenase (LDH), while reoxygenation not only further increased the apoptotic rates and leakage of LDH, but also induced necrosis of cardiomyocytes. In addition, hypoxia increased the levels of NO2 -/NO3 - and thiobarbituric acid reacted substances (TBARS), while reoxygenation decreased NO2 -/NO3 -, but further increased TBARS in the cultured media. Moreover, hypoxia up-regulated the expression levels of bcl-2 and p53 proteins, while reoxygenation down-regulated bcl-2 and further up-regulated p53. Chinonin significantly decreased the rates of apoptotic and necrotic cardiomyocytes, and inhibited the leakage of LDH. It also diminished NO2 -/NO3 - and TBARS, down-regulated the expression level of p53 protein, and up-regulated bcl-2 protein, respectively. The results suggest that Chinonin has preventive effects against apoptotic and necrotic cell death and its protective mechanisms are related to the antioxidant properties of scavenging nitric oxide and oxygen free radicals, and the modulating effects on the expression levels of bcl-2 and p53 proteins. Copyright (C) 2000 Elsevier Science B.V.
Persistent Identifierhttp://hdl.handle.net/10722/179406
ISSN
2015 Impact Factor: 5.158
2015 SCImago Journal Rankings: 2.718
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorShen, JGen_US
dc.contributor.authorQuo, XSen_US
dc.contributor.authorJiang, Ben_US
dc.contributor.authorLi, Men_US
dc.contributor.authorXin, WJen_US
dc.contributor.authorZhao, BLen_US
dc.date.accessioned2012-12-19T09:56:13Z-
dc.date.available2012-12-19T09:56:13Z-
dc.date.issued2000en_US
dc.identifier.citationBiochimica Et Biophysica Acta - Molecular Basis Of Disease, 2000, v. 1500 n. 2, p. 217-226en_US
dc.identifier.issn0925-4439en_US
dc.identifier.urihttp://hdl.handle.net/10722/179406-
dc.description.abstractThe inhibitory effects of Chinonin, a natural antioxidant extracted from a Chinese medicine, on apoptotic and necrotic cell death of cardiomyocytes in hypoxia-reoxygenation process were observed in this study. The possible mechanisms of Chinonin on scavenging reactive oxygen species and regulating apoptotic related genes bcl-2 and p53 were also investigated. Neonatal rat cardiomyocytes were subjected to 24-h hypoxia and 4-h reoxygenation. Cell death was evaluated by DNA electrophoresis on agarose gel, cell death ELISA and annexin-V-FLUOS/propidium iodide (PI) double staining cytometry. Hypoxia caused the increase of apoptotic rates and the release of lactate dehydrogenase (LDH), while reoxygenation not only further increased the apoptotic rates and leakage of LDH, but also induced necrosis of cardiomyocytes. In addition, hypoxia increased the levels of NO2 -/NO3 - and thiobarbituric acid reacted substances (TBARS), while reoxygenation decreased NO2 -/NO3 -, but further increased TBARS in the cultured media. Moreover, hypoxia up-regulated the expression levels of bcl-2 and p53 proteins, while reoxygenation down-regulated bcl-2 and further up-regulated p53. Chinonin significantly decreased the rates of apoptotic and necrotic cardiomyocytes, and inhibited the leakage of LDH. It also diminished NO2 -/NO3 - and TBARS, down-regulated the expression level of p53 protein, and up-regulated bcl-2 protein, respectively. The results suggest that Chinonin has preventive effects against apoptotic and necrotic cell death and its protective mechanisms are related to the antioxidant properties of scavenging nitric oxide and oxygen free radicals, and the modulating effects on the expression levels of bcl-2 and p53 proteins. Copyright (C) 2000 Elsevier Science B.V.en_US
dc.languageengen_US
dc.publisherElsevier BV. The Journal's web site is located at http://www.elsevier.com/locate/bbadisen_US
dc.relation.ispartofBiochimica et Biophysica Acta - Molecular Basis of Diseaseen_US
dc.subject.meshAnimalsen_US
dc.subject.meshAnimals, Newbornen_US
dc.subject.meshAnnexin A5 - Analysisen_US
dc.subject.meshApoptosis - Drug Effectsen_US
dc.subject.meshBiological Markersen_US
dc.subject.meshCell Hypoxiaen_US
dc.subject.meshCells, Cultureden_US
dc.subject.meshDna Fragmentation - Drug Effectsen_US
dc.subject.meshEnzyme-Linked Immunosorbent Assayen_US
dc.subject.meshFlow Cytometryen_US
dc.subject.meshFree Radical Scavengers - Pharmacologyen_US
dc.subject.meshGenes, Bcl-2en_US
dc.subject.meshGenes, P53en_US
dc.subject.meshGlycosides - Pharmacologyen_US
dc.subject.meshHeart - Drug Effectsen_US
dc.subject.meshL-Lactate Dehydrogenase - Analysisen_US
dc.subject.meshLipid Peroxidation - Drug Effectsen_US
dc.subject.meshMyocardial Ischemia - Pathologyen_US
dc.subject.meshMyocardial Reperfusion Injury - Pathologyen_US
dc.subject.meshMyocardium - Pathologyen_US
dc.subject.meshNecrosisen_US
dc.subject.meshNitrates - Analysisen_US
dc.subject.meshNitric Oxide - Metabolismen_US
dc.subject.meshNitrites - Analysisen_US
dc.subject.meshRatsen_US
dc.subject.meshRats, Wistaren_US
dc.subject.meshReactive Oxygen Speciesen_US
dc.subject.meshThiobarbituric Acid Reactive Substances - Analysisen_US
dc.subject.meshXanthenes - Pharmacologyen_US
dc.titleChinonin, a novel drug against cardiomyocyte apoptosis induced by hypoxia and reoxygenationen_US
dc.typeArticleen_US
dc.identifier.emailShen, JG: shenjg@hku.hken_US
dc.identifier.authorityShen, JG=rp00487en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.1016/S0925-4439(99)00109-Xen_US
dc.identifier.pmid10657591-
dc.identifier.scopuseid_2-s2.0-0033972024en_US
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-0033972024&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume1500en_US
dc.identifier.issue2en_US
dc.identifier.spage217en_US
dc.identifier.epage226en_US
dc.identifier.isiWOS:000085469800008-
dc.publisher.placeNetherlandsen_US
dc.identifier.scopusauthoridShen, JG=7404929947en_US
dc.identifier.scopusauthoridQuo, XS=6603006564en_US
dc.identifier.scopusauthoridJiang, B=34770534200en_US
dc.identifier.scopusauthoridLi, M=36066390600en_US
dc.identifier.scopusauthoridXin, WJ=7102977683en_US
dc.identifier.scopusauthoridZhao, BL=7403058931en_US

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