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Article: Salvianolic acid B inhibits hydrogen peroxide-induced endothelial cell apoptosis through regulating PI3K/Akt signaling
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TitleSalvianolic acid B inhibits hydrogen peroxide-induced endothelial cell apoptosis through regulating PI3K/Akt signaling
 
AuthorsLiu, CL1 3
Xie, LX3
Li, M3
Durairajan, SSK3
Goto, S2
Huang, JD1
 
Issue Date2007
 
PublisherPublic Library of Science. The Journal's web site is located at http://www.plosone.org/home.action
 
CitationPlos One, 2007, v. 2 n. 12 [How to Cite?]
DOI: http://dx.doi.org/10.1371/journal.pone.0001321
 
AbstractBackground. Salvianolic acid B (Sal B) is one of the most bioactive components of Salvia miltiorrhiza, a traditional Chinese herbal medicine that has been commonly used for prevention and treatment of cerebrovascular disorders. However, the mechanism responsible for such protective effects remains largely unknown. It has been considered that cerebral endothelium apoptosis caused by reactive oxygen species including hydrogen peroxide (H2O2) is implicated in the pathogenesis of cerebrovascular disorders. Methodology and Principal Findings. By examining the effect of Sal B on H2O2-induced apoptosis in rat cerebral microvascular endothelial cells (rCMECs), we found that Sal B pretreatment significantly attenuated H2O2-induced apoptosis in rCMECs. We next examined the signaling cascade(s) involved in Sal B-mediated anti-apoptotic effects. We showed that H2O2 induces rCMECs apoptosis mainly through the PI3K/ERK pathway, since a PI3K inhibitor (LY294002) blocked ERK activation caused by H2O2 and a specific inhibitor of MEK (U0126) protected cells from apoptosis. On the other hand, blockage of the PI3K/Akt pathway abrogated the protective effect conferred by Sal B and potentated H2O2-induced apoptosis, suggesting that Sal B prevents H2O2-induced apoptosis predominantly through the PI3K/Akt (upstream of ERK) pathway. Significance. Our findings provide the first evidence that H2 O2 induces rCMECs apoptosis via the PI3K/MEK/ERK pathway and that Sal B protects rCMECs against H2O2-induced apoptosis through the PI3K/Akt/Raf/MEK/ERK pathway. © 2007 Liu et al.
 
ISSN1932-6203
2013 Impact Factor: 3.534
2013 SCImago Journal Rankings: 1.724
 
DOIhttp://dx.doi.org/10.1371/journal.pone.0001321
 
PubMed Central IDPMC2117346
 
ISI Accession Number IDWOS:000207459600009
Funding AgencyGrant Number
Research Grant Council of Hong KongHKU 7636/05M
Hong Kong Baptist UniversityFRG/06-07/I-07
FRG/06-07/II-43
Funding Information:

This work was supported by a grant (HKU 7636/05M) from the Research Grant Council of Hong Kong awarded to Dr. J.D. Huang, and was also supported by grants (FRG/06-07/I-07 and FRG/06-07/II-43) from Hong Kong Baptist University awarded to Dr. M. Li. The funders had no roles in the design and conduct of the study, in the collection, analysis, and interpretation of the data, and in the preparation, review, or approval of the manuscript.

 
ReferencesReferences in Scopus
 
GrantsRole of kinesin-mediated intracellular transportation in Alzheimer's Disease
 
DC FieldValue
dc.contributor.authorLiu, CL
 
dc.contributor.authorXie, LX
 
dc.contributor.authorLi, M
 
dc.contributor.authorDurairajan, SSK
 
dc.contributor.authorGoto, S
 
dc.contributor.authorHuang, JD
 
dc.date.accessioned2010-09-06T06:02:00Z
 
dc.date.available2010-09-06T06:02:00Z
 
dc.date.issued2007
 
dc.description.abstractBackground. Salvianolic acid B (Sal B) is one of the most bioactive components of Salvia miltiorrhiza, a traditional Chinese herbal medicine that has been commonly used for prevention and treatment of cerebrovascular disorders. However, the mechanism responsible for such protective effects remains largely unknown. It has been considered that cerebral endothelium apoptosis caused by reactive oxygen species including hydrogen peroxide (H2O2) is implicated in the pathogenesis of cerebrovascular disorders. Methodology and Principal Findings. By examining the effect of Sal B on H2O2-induced apoptosis in rat cerebral microvascular endothelial cells (rCMECs), we found that Sal B pretreatment significantly attenuated H2O2-induced apoptosis in rCMECs. We next examined the signaling cascade(s) involved in Sal B-mediated anti-apoptotic effects. We showed that H2O2 induces rCMECs apoptosis mainly through the PI3K/ERK pathway, since a PI3K inhibitor (LY294002) blocked ERK activation caused by H2O2 and a specific inhibitor of MEK (U0126) protected cells from apoptosis. On the other hand, blockage of the PI3K/Akt pathway abrogated the protective effect conferred by Sal B and potentated H2O2-induced apoptosis, suggesting that Sal B prevents H2O2-induced apoptosis predominantly through the PI3K/Akt (upstream of ERK) pathway. Significance. Our findings provide the first evidence that H2 O2 induces rCMECs apoptosis via the PI3K/MEK/ERK pathway and that Sal B protects rCMECs against H2O2-induced apoptosis through the PI3K/Akt/Raf/MEK/ERK pathway. © 2007 Liu et al.
 
dc.description.naturepublished_or_final_version
 
dc.identifier.citationPlos One, 2007, v. 2 n. 12 [How to Cite?]
DOI: http://dx.doi.org/10.1371/journal.pone.0001321
 
dc.identifier.citeulike2221465
 
dc.identifier.doihttp://dx.doi.org/10.1371/journal.pone.0001321
 
dc.identifier.hkuros146695
 
dc.identifier.isiWOS:000207459600009
Funding AgencyGrant Number
Research Grant Council of Hong KongHKU 7636/05M
Hong Kong Baptist UniversityFRG/06-07/I-07
FRG/06-07/II-43
Funding Information:

This work was supported by a grant (HKU 7636/05M) from the Research Grant Council of Hong Kong awarded to Dr. J.D. Huang, and was also supported by grants (FRG/06-07/I-07 and FRG/06-07/II-43) from Hong Kong Baptist University awarded to Dr. M. Li. The funders had no roles in the design and conduct of the study, in the collection, analysis, and interpretation of the data, and in the preparation, review, or approval of the manuscript.

 
dc.identifier.issn1932-6203
2013 Impact Factor: 3.534
2013 SCImago Journal Rankings: 1.724
 
dc.identifier.issue12
 
dc.identifier.openurl
 
dc.identifier.pmcidPMC2117346
 
dc.identifier.pmid18091994
 
dc.identifier.scopuseid_2-s2.0-44449179744
 
dc.identifier.urihttp://hdl.handle.net/10722/68168
 
dc.identifier.volume2
 
dc.languageeng
 
dc.publisherPublic Library of Science. The Journal's web site is located at http://www.plosone.org/home.action
 
dc.publisher.placeUnited States
 
dc.relation.ispartofPLoS ONE
 
dc.relation.projectRole of kinesin-mediated intracellular transportation in Alzheimer's Disease
 
dc.relation.referencesReferences in Scopus
 
dc.rightsCreative Commons: Attribution 3.0 Hong Kong License
 
dc.subject.meshApoptosis - drug effects
 
dc.subject.meshBenzofurans - pharmacology
 
dc.subject.meshEndothelium, Vascular - cytology - drug effects - enzymology
 
dc.subject.meshHydrogen Peroxide - pharmacology
 
dc.subject.meshPhosphatidylinositol 3-Kinases - metabolism
 
dc.titleSalvianolic acid B inhibits hydrogen peroxide-induced endothelial cell apoptosis through regulating PI3K/Akt signaling
 
dc.typeArticle
 
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Author Affiliations
  1. The University of Hong Kong Li Ka Shing Faculty of Medicine
  2. Tokai University
  3. Hong Kong Baptist University