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Article: Plant Natural Product Formononetin Protects Rat Cardiomyocyte H9c2 Cells against Oxygen Glucose Deprivation and Reoxygenation via Inhibiting ROS Formation and Promoting GSK-3β Phosphorylation

TitlePlant Natural Product Formononetin Protects Rat Cardiomyocyte H9c2 Cells against Oxygen Glucose Deprivation and Reoxygenation via Inhibiting ROS Formation and Promoting GSK-3β Phosphorylation
Authors
Issue Date2016
PublisherHindawi Publishing Corporation. The Journal's web site is located at http://www.hindawi.com/journals/oximed/
Citation
Oxidative Medicine and Cellular Longevity, 2016, v. 2016, article no. 2060874 How to Cite?
AbstractThe opening of mitochondrial permeability transition pore (mPTP) is a major cause of cell death in ischemia reperfusion injury. Based on our pilot experiments, plant natural product formononetin enhanced the survival of rat cardiomyocyte H9c2 cells during oxygen glucose deprivation (OGD) and reoxygenation. For mechanistic studies, we focused on two major cellular factors, namely, reactive oxygen species (ROS) and glycogen synthase kinase 3β (GSK-3β), in the regulation of mPTP opening. We found that formononetin suppressed the formation of ROS and superoxide in a concentration-dependent manner. Formononetin also rescued OGD/reoxygenation-induced loss of mitochondrial membrane integrity. Further studies suggested that formononetin induced Akt activation and GSK-3β (Ser9) phosphorylation, thereby reducing GSK-3β activity towards mPTP opening. PI3K and PKC inhibitors abolished the effects of formononetin on mPTP opening and GSK-3β phosphorylation. Immunoprecipitation experiments further revealed that formononetin increased the binding of phosphor-GSK-3β to adenine nucleotide translocase (ANT) while it disrupted the complex of ANT with cyclophilin D. Moreover, immunofluorescence revealed that phospho-GSK-3β (Ser9) was mainly deposited in the space between mitochondria and cell nucleus. Collectively, these results indicated that formononetin protected cardiomyocytes from OGD/reoxygenation injury via inhibiting ROS formation and promoting GSK-3β phosphorylation.
Persistent Identifierhttp://hdl.handle.net/10722/225612
ISSN
2015 Impact Factor: 4.492
2015 SCImago Journal Rankings: 1.503
PubMed Central ID

 

DC FieldValueLanguage
dc.contributor.authorCheng, Y-
dc.contributor.authorXia, Z-
dc.contributor.authorHan, Y-
dc.contributor.authorRong, J-
dc.date.accessioned2016-05-20T08:09:21Z-
dc.date.available2016-05-20T08:09:21Z-
dc.date.issued2016-
dc.identifier.citationOxidative Medicine and Cellular Longevity, 2016, v. 2016, article no. 2060874-
dc.identifier.issn1942-0900-
dc.identifier.urihttp://hdl.handle.net/10722/225612-
dc.description.abstractThe opening of mitochondrial permeability transition pore (mPTP) is a major cause of cell death in ischemia reperfusion injury. Based on our pilot experiments, plant natural product formononetin enhanced the survival of rat cardiomyocyte H9c2 cells during oxygen glucose deprivation (OGD) and reoxygenation. For mechanistic studies, we focused on two major cellular factors, namely, reactive oxygen species (ROS) and glycogen synthase kinase 3β (GSK-3β), in the regulation of mPTP opening. We found that formononetin suppressed the formation of ROS and superoxide in a concentration-dependent manner. Formononetin also rescued OGD/reoxygenation-induced loss of mitochondrial membrane integrity. Further studies suggested that formononetin induced Akt activation and GSK-3β (Ser9) phosphorylation, thereby reducing GSK-3β activity towards mPTP opening. PI3K and PKC inhibitors abolished the effects of formononetin on mPTP opening and GSK-3β phosphorylation. Immunoprecipitation experiments further revealed that formononetin increased the binding of phosphor-GSK-3β to adenine nucleotide translocase (ANT) while it disrupted the complex of ANT with cyclophilin D. Moreover, immunofluorescence revealed that phospho-GSK-3β (Ser9) was mainly deposited in the space between mitochondria and cell nucleus. Collectively, these results indicated that formononetin protected cardiomyocytes from OGD/reoxygenation injury via inhibiting ROS formation and promoting GSK-3β phosphorylation.-
dc.languageeng-
dc.publisherHindawi Publishing Corporation. The Journal's web site is located at http://www.hindawi.com/journals/oximed/-
dc.relation.ispartofOxidative Medicine and Cellular Longevity-
dc.rightsCreative Commons: Attribution 3.0 Hong Kong License-
dc.titlePlant Natural Product Formononetin Protects Rat Cardiomyocyte H9c2 Cells against Oxygen Glucose Deprivation and Reoxygenation via Inhibiting ROS Formation and Promoting GSK-3β Phosphorylation-
dc.typeArticle-
dc.identifier.emailXia, Z: zyxia@hkucc.hku.hk-
dc.identifier.emailRong, J: jrong@hku.hk-
dc.identifier.authorityXia, Z=rp00532-
dc.identifier.authorityRong, J=rp00515-
dc.description.naturepublished_or_final_version-
dc.identifier.doi10.1155/2016/2060874-
dc.identifier.pmid27034732-
dc.identifier.pmcidPMC4806648-
dc.identifier.hkuros257879-
dc.identifier.volume2016-
dc.publisher.placeUnited States-

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