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Article: Potential roles of PI3K/Akt and Nrf2-Keap1 pathways in regulating hormesis of Z-ligustilide in PC12 cells against oxygen and glucose deprivation

TitlePotential roles of PI3K/Akt and Nrf2-Keap1 pathways in regulating hormesis of Z-ligustilide in PC12 cells against oxygen and glucose deprivation
Authors
Issue Date2012
PublisherPergamon. The Journal's web site is located at http://www.elsevier.com/locate/neuropharm
Citation
Neuropharmacology, 2012, v. 62 n. 4, p. 1659-1670 How to Cite?
AbstractMany phytochemicals may ameliorate neurological disorders through a hormetic mechanism. The aim of this study was to characterize the hormetic role of Z-ligustilide in PC12 cells against oxygen glucose deprivation (OGD) induced cell death. We examined the interactions of Z-ligustilide with the pro-survival signals mediated by phosphatidylinositol 3-kinase (PI3K) and transcription factor nuclear factor-erythroid 2 p45-related factor 2 (Nrf2) pathways. We also investigated the effect of Z-ligustilide on the intracellular redox signaling system involving reactive oxygen species (ROS) and glutathione (GSH). Z-ligustilide not only triggered stress response by causing ROS formation and transient GSH depletion, but also activated survival-promoting signals via cross-talking of PI3K and Nrf2 pathways. A key finding was that Z-ligustilide preconditioning protected PC12 cells from OGD-induced injury either at a low concentration for a prolonged period of time or at a high concentration for a short period of time. Presumably, mild preconditioning stimulated moderate ROS production, but effectively activated hormetic signals and induced stress responsive genes. In contrast, higher concentrations of Z-ligustilide could be toxic over a prolonged period of time due to massive ROS production. These results suggest that the effect of Z-ligustilide may be regulated by a biphasic hormetic mechanism involving initial induction of oxidative stress and subsequent activation of stress response gene expression. © 2011 Elsevier Ltd. All rights reserved.
Persistent Identifierhttp://hdl.handle.net/10722/160719
ISSN
2015 Impact Factor: 4.936
2015 SCImago Journal Rankings: 2.506
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorQi, Hen_HK
dc.contributor.authorHan, Yen_HK
dc.contributor.authorRong, Jen_HK
dc.date.accessioned2012-08-16T06:17:19Z-
dc.date.available2012-08-16T06:17:19Z-
dc.date.issued2012en_HK
dc.identifier.citationNeuropharmacology, 2012, v. 62 n. 4, p. 1659-1670en_HK
dc.identifier.issn0028-3908en_HK
dc.identifier.urihttp://hdl.handle.net/10722/160719-
dc.description.abstractMany phytochemicals may ameliorate neurological disorders through a hormetic mechanism. The aim of this study was to characterize the hormetic role of Z-ligustilide in PC12 cells against oxygen glucose deprivation (OGD) induced cell death. We examined the interactions of Z-ligustilide with the pro-survival signals mediated by phosphatidylinositol 3-kinase (PI3K) and transcription factor nuclear factor-erythroid 2 p45-related factor 2 (Nrf2) pathways. We also investigated the effect of Z-ligustilide on the intracellular redox signaling system involving reactive oxygen species (ROS) and glutathione (GSH). Z-ligustilide not only triggered stress response by causing ROS formation and transient GSH depletion, but also activated survival-promoting signals via cross-talking of PI3K and Nrf2 pathways. A key finding was that Z-ligustilide preconditioning protected PC12 cells from OGD-induced injury either at a low concentration for a prolonged period of time or at a high concentration for a short period of time. Presumably, mild preconditioning stimulated moderate ROS production, but effectively activated hormetic signals and induced stress responsive genes. In contrast, higher concentrations of Z-ligustilide could be toxic over a prolonged period of time due to massive ROS production. These results suggest that the effect of Z-ligustilide may be regulated by a biphasic hormetic mechanism involving initial induction of oxidative stress and subsequent activation of stress response gene expression. © 2011 Elsevier Ltd. All rights reserved.en_HK
dc.languageengen_US
dc.publisherPergamon. The Journal's web site is located at http://www.elsevier.com/locate/neuropharmen_HK
dc.relation.ispartofNeuropharmacologyen_HK
dc.subject.mesh4-Butyrolactone - analogs & derivatives - pharmacologyen_HK
dc.subject.meshAnimalsen_HK
dc.subject.meshAnoxia - metabolismen_HK
dc.subject.meshGlucose - deficiencyen_HK
dc.subject.meshHeme Oxygenase-1 - metabolismen_HK
dc.subject.meshHormesis - physiologyen_HK
dc.subject.meshNF-E2-Related Factor 2 - metabolismen_HK
dc.subject.meshOxidative Stress - drug effectsen_HK
dc.subject.meshPC12 Cellsen_HK
dc.subject.meshPhosphatidylinositol 3-Kinases - metabolismen_HK
dc.subject.meshProteins - metabolismen_HK
dc.subject.meshProto-Oncogene Proteins c-akt - metabolismen_HK
dc.subject.meshRatsen_HK
dc.subject.meshReactive Oxygen Species - metabolismen_HK
dc.subject.meshSignal Transduction - drug effectsen_HK
dc.titlePotential roles of PI3K/Akt and Nrf2-Keap1 pathways in regulating hormesis of Z-ligustilide in PC12 cells against oxygen and glucose deprivationen_HK
dc.typeArticleen_HK
dc.identifier.emailRong, J: jrong@hku.hken_HK
dc.identifier.authorityRong, J=rp00515en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1016/j.neuropharm.2011.11.012en_HK
dc.identifier.pmid22146407-
dc.identifier.scopuseid_2-s2.0-84856429809en_HK
dc.identifier.hkuros203764en_US
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-84856429809&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume62en_HK
dc.identifier.issue4en_HK
dc.identifier.spage1659en_HK
dc.identifier.epage1670en_HK
dc.identifier.eissn1873-7064-
dc.identifier.isiWOS:000301221500007-
dc.publisher.placeUnited Kingdomen_HK
dc.identifier.scopusauthoridQi, H=35367105300en_HK
dc.identifier.scopusauthoridHan, Y=8527680500en_HK
dc.identifier.scopusauthoridRong, J=7005980047en_HK
dc.identifier.citeulike10103162-

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