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Article: Lycopene protects against hypoxia/reoxygenation-induced apoptosis by preventing mitochondrial dysfunction in primary neonatal mouse cardiomyocytes

TitleLycopene protects against hypoxia/reoxygenation-induced apoptosis by preventing mitochondrial dysfunction in primary neonatal mouse cardiomyocytes
Authors
KeywordsAnimals
Animals, Newborn
Apoptosis/*drug effects
Carotenoids/*pharmacology
Cell Hypoxia/drug effects
Cell Survival/drug effects
Cytoprotection/*drug effects
Mice
Mice, Inbred C57BL
Mitochondria/*drug effects/metabolism
Mitochondrial Membrane Transport Proteins/chemistry/metabolism
Myocytes, Cardiac/*cytology/*drug effects/metabolism
Oxidative Stress/drug effects
Oxygen/*metabolism
Protein Conformation/drug effects
Signal Transduction/drug effects
Issue Date2012
PublisherPublic Library of Science. The Journal's web site is located at http://www.plosone.org/home.action
Citation
PLoS One, 2012, v. 7 n. 11, p. article no. e50778 How to Cite?
AbstractBACKGROUND: Hypoxia/reoxygenation(H/R)-induced apoptosis of cardiomyocytes plays an important role in myocardial injury. Lycopene is a potent antioxidant carotenoid that has been shown to have protective properties on cardiovascular system. The aim of the present study is to investigate the potential for lycopene to protect the cardiomyocytes exposed to H/R. Moreover, the effect on mitochondrial function upon lycopene exposure was assessed. METHODS AND FINDINGS: Primary cardiomyocytes were isolated from neonatal mouse and established an in vitro model of H/R which resembles ischemia/reperfusion in vivo. The pretreatment of cardiomyocytes with 5 microM lycopene significantly reduced the extent of apoptosis detected by TUNEL assays. To further study the mechanism underlying the benefits of lycopene, interactions between lycopene and the process of mitochondria-mediated apoptosis were examined. Lycopene pretreatment of cardiomyocytes suppressed the activation of the mitochondrial permeability transition pore (mPTP) by reducing the intracellular reactive oxygen species (ROS) levels and inhibiting the increase of malondialdehyde (MDA) levels caused by H/R. Moreover, the loss of mitochondrial membrane potential, a decline in cellular ATP levels, a reduction in the amount of cytochrome c translocated to the cytoplasm and caspase-3 activation were observed in lycopene-treated cultures. CONCLUSION: The present results suggested that lycopene possesses great pharmacological potential in protecting against H/R-induced apoptosis. Importantly, the protective effects of lycopene may be attributed to its roles in improving mitochondrial function in H/R-treated cardiomyocytes.
Persistent Identifierhttp://hdl.handle.net/10722/207694
ISSN
2015 Impact Factor: 3.057
2015 SCImago Journal Rankings: 1.395
PubMed Central ID

 

DC FieldValueLanguage
dc.contributor.authorYue, Ren_US
dc.contributor.authorHu, Hen_US
dc.contributor.authorYiu, KHen_US
dc.contributor.authorLuo, Ten_US
dc.contributor.authorZhou, Zen_US
dc.contributor.authorXu, Len_US
dc.contributor.authorZhang, Sen_US
dc.contributor.authorLi, Ken_US
dc.contributor.authorYu, Zen_US
dc.date.accessioned2015-01-19T04:20:25Z-
dc.date.available2015-01-19T04:20:25Z-
dc.date.issued2012en_US
dc.identifier.citationPLoS One, 2012, v. 7 n. 11, p. article no. e50778en_US
dc.identifier.issn1932-6203en_US
dc.identifier.urihttp://hdl.handle.net/10722/207694-
dc.description.abstractBACKGROUND: Hypoxia/reoxygenation(H/R)-induced apoptosis of cardiomyocytes plays an important role in myocardial injury. Lycopene is a potent antioxidant carotenoid that has been shown to have protective properties on cardiovascular system. The aim of the present study is to investigate the potential for lycopene to protect the cardiomyocytes exposed to H/R. Moreover, the effect on mitochondrial function upon lycopene exposure was assessed. METHODS AND FINDINGS: Primary cardiomyocytes were isolated from neonatal mouse and established an in vitro model of H/R which resembles ischemia/reperfusion in vivo. The pretreatment of cardiomyocytes with 5 microM lycopene significantly reduced the extent of apoptosis detected by TUNEL assays. To further study the mechanism underlying the benefits of lycopene, interactions between lycopene and the process of mitochondria-mediated apoptosis were examined. Lycopene pretreatment of cardiomyocytes suppressed the activation of the mitochondrial permeability transition pore (mPTP) by reducing the intracellular reactive oxygen species (ROS) levels and inhibiting the increase of malondialdehyde (MDA) levels caused by H/R. Moreover, the loss of mitochondrial membrane potential, a decline in cellular ATP levels, a reduction in the amount of cytochrome c translocated to the cytoplasm and caspase-3 activation were observed in lycopene-treated cultures. CONCLUSION: The present results suggested that lycopene possesses great pharmacological potential in protecting against H/R-induced apoptosis. Importantly, the protective effects of lycopene may be attributed to its roles in improving mitochondrial function in H/R-treated cardiomyocytes.en_US
dc.languageengen_US
dc.publisherPublic Library of Science. The Journal's web site is located at http://www.plosone.org/home.actionen_US
dc.relation.ispartofPLoS Oneen_US
dc.rightsCreative Commons: Attribution 3.0 Hong Kong License-
dc.subjectAnimalsen_US
dc.subjectAnimals, Newbornen_US
dc.subjectApoptosis/*drug effectsen_US
dc.subjectCarotenoids/*pharmacologyen_US
dc.subjectCell Hypoxia/drug effectsen_US
dc.subjectCell Survival/drug effectsen_US
dc.subjectCytoprotection/*drug effectsen_US
dc.subjectMiceen_US
dc.subjectMice, Inbred C57BLen_US
dc.subjectMitochondria/*drug effects/metabolismen_US
dc.subjectMitochondrial Membrane Transport Proteins/chemistry/metabolismen_US
dc.subjectMyocytes, Cardiac/*cytology/*drug effects/metabolismen_US
dc.subjectOxidative Stress/drug effectsen_US
dc.subjectOxygen/*metabolismen_US
dc.subjectProtein Conformation/drug effectsen_US
dc.subjectSignal Transduction/drug effectsen_US
dc.titleLycopene protects against hypoxia/reoxygenation-induced apoptosis by preventing mitochondrial dysfunction in primary neonatal mouse cardiomyocytesen_US
dc.typeArticleen_US
dc.identifier.emailYiu, KH: khkyiu@hku.hken_US
dc.identifier.authorityYiu, KH=rp01490en_US
dc.description.naturepublished_or_final_version-
dc.identifier.doi10.1371/journal.pone.0050778en_US
dc.identifier.pmid23226382-
dc.identifier.pmcidPMC3511264-
dc.identifier.hkuros254870-
dc.identifier.volume7en_US
dc.identifier.issue11en_US
dc.identifier.spagearticle no. e50778en_US
dc.identifier.epagearticle no. e50778en_US

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