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Article: Salvianolic acid B inhibits hydrogen peroxide-induced endothelial cell apoptosis through regulating PI3K/Akt signaling

TitleSalvianolic acid B inhibits hydrogen peroxide-induced endothelial cell apoptosis through regulating PI3K/Akt signaling
Authors
Issue Date2007
PublisherPublic Library of Science. The Journal's web site is located at http://www.plosone.org/home.action
Citation
Plos One, 2007, v. 2 n. 12 How to Cite?
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.
Persistent Identifierhttp://hdl.handle.net/10722/68168
ISSN
2014 Impact Factor: 3.234
2014 SCImago Journal Rankings: 1.300
PubMed Central ID
ISI Accession Number ID
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.

References
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DC FieldValueLanguage
dc.contributor.authorLiu, CLen_HK
dc.contributor.authorXie, LXen_HK
dc.contributor.authorLi, Men_HK
dc.contributor.authorDurairajan, SSKen_HK
dc.contributor.authorGoto, Sen_HK
dc.contributor.authorHuang, JDen_HK
dc.date.accessioned2010-09-06T06:02:00Z-
dc.date.available2010-09-06T06:02:00Z-
dc.date.issued2007en_HK
dc.identifier.citationPlos One, 2007, v. 2 n. 12en_HK
dc.identifier.issn1932-6203en_HK
dc.identifier.urihttp://hdl.handle.net/10722/68168-
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.en_HK
dc.languageengen_HK
dc.publisherPublic Library of Science. The Journal's web site is located at http://www.plosone.org/home.actionen_HK
dc.relation.ispartofPLoS ONEen_HK
dc.rightsCreative Commons: Attribution 3.0 Hong Kong Licenseen_HK
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 signalingen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=1932-6203&volume=2&issue=12&spage=1321&epage=&date=2007&atitle=Salvianolic+Acid+B+Inhibits+Hydrogen+Peroxide-Induced+Endothelial+Cell+Apoptosis+through+Regulating+PI3K/Akt+Signaling.en_HK
dc.identifier.emailHuang, JD:jdhuang@hkucc.hku.hken_HK
dc.identifier.authorityHuang, JD=rp00451en_HK
dc.description.naturepublished_or_final_version-
dc.identifier.doi10.1371/journal.pone.0001321en_HK
dc.identifier.pmid18091994en_HK
dc.identifier.pmcidPMC2117346-
dc.identifier.scopuseid_2-s2.0-44449179744en_HK
dc.identifier.hkuros146695en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-44449179744&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume2en_HK
dc.identifier.issue12en_HK
dc.identifier.isiWOS:000207459600009-
dc.publisher.placeUnited Statesen_HK
dc.relation.projectRole of kinesin-mediated intracellular transportation in Alzheimer's Disease-
dc.identifier.scopusauthoridLiu, CL=24503690100en_HK
dc.identifier.scopusauthoridXie, LX=23483050700en_HK
dc.identifier.scopusauthoridLi, M=36071647500en_HK
dc.identifier.scopusauthoridDurairajan, SSK=23469201000en_HK
dc.identifier.scopusauthoridGoto, S=7403437579en_HK
dc.identifier.scopusauthoridHuang, JD=8108660600en_HK
dc.identifier.citeulike2221465-

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