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Article: Icaritin protects against oxidative stress-induced injury in cardiac H9c2 cells via Akt/Nrf2/HO-1 and calcium signalling pathways

TitleIcaritin protects against oxidative stress-induced injury in cardiac H9c2 cells via Akt/Nrf2/HO-1 and calcium signalling pathways
Authors
KeywordsIcaritin
Cardiac H9c2 cells
Oxidative stress
NF-E2-related factor 2
Calcium ion
Issue Date2015
PublisherElsevier BV. The Journal's web site is located at http://www.elsevier.com/wps/find/journaldescription.cws_home/717426/description#description
Citation
Journal of Functional Foods, 2015, v. 18 n. Pt. A, p. 213-223 How to Cite?
AbstractIcaritin, a prenylflavonoid isolated from Herbal Epimedii, is well known for its osteoplastic and anti-tumour activities. Here, we examined the cardioprotective actions of icaritin on cardiac H9c2 cells under oxidative stress conditions induced by treatment with tert-butylhydroperoxide (t-BHP). Icaritin at a concentration range between 1 and 4 µM effectively increased cell viability and decreased lactate dehydrogenase (LDH) leakage and reactive oxygen species (ROS) release in t-BHP treated cells, reflecting its ability to reduce t-BHP-induced cell injury. Icaritin also protected cell membrane integrity by preventing the collapse of the mitochondrial membrane potential. In addition, pretreatment of NF-E2-related factor 2 (Nrf2) siRNA and Akt inhibitor abolished the cardioprotective effect of icaritin. Furthermore, Nrf2 siRNA transfection interfered with the effect of icaritin on the inhibition of Ca2+ overload, whereas Akt inhibitor reduced icaritin-induced haemo-oxygenase-1 (HO-1) expression. Collectively, these results suggest that icaritin exerted its cardioprotective effect through the Akt/Nrf2/HO-1 and calcium signalling pathways.
Persistent Identifierhttp://hdl.handle.net/10722/271259
ISSN
2017 Impact Factor: 3.47
2015 SCImago Journal Rankings: 1.346

 

DC FieldValueLanguage
dc.contributor.authorLei, SW-
dc.contributor.authorCui, G-
dc.contributor.authorLeung, GPH-
dc.contributor.authorLuk, SCW-
dc.contributor.authorHoi, MPM-
dc.contributor.authorWang, L-
dc.contributor.authorMahady, GB-
dc.contributor.authorLee, SMY-
dc.date.accessioned2019-06-24T01:06:26Z-
dc.date.available2019-06-24T01:06:26Z-
dc.date.issued2015-
dc.identifier.citationJournal of Functional Foods, 2015, v. 18 n. Pt. A, p. 213-223-
dc.identifier.issn1756-4646-
dc.identifier.urihttp://hdl.handle.net/10722/271259-
dc.description.abstractIcaritin, a prenylflavonoid isolated from Herbal Epimedii, is well known for its osteoplastic and anti-tumour activities. Here, we examined the cardioprotective actions of icaritin on cardiac H9c2 cells under oxidative stress conditions induced by treatment with tert-butylhydroperoxide (t-BHP). Icaritin at a concentration range between 1 and 4 µM effectively increased cell viability and decreased lactate dehydrogenase (LDH) leakage and reactive oxygen species (ROS) release in t-BHP treated cells, reflecting its ability to reduce t-BHP-induced cell injury. Icaritin also protected cell membrane integrity by preventing the collapse of the mitochondrial membrane potential. In addition, pretreatment of NF-E2-related factor 2 (Nrf2) siRNA and Akt inhibitor abolished the cardioprotective effect of icaritin. Furthermore, Nrf2 siRNA transfection interfered with the effect of icaritin on the inhibition of Ca2+ overload, whereas Akt inhibitor reduced icaritin-induced haemo-oxygenase-1 (HO-1) expression. Collectively, these results suggest that icaritin exerted its cardioprotective effect through the Akt/Nrf2/HO-1 and calcium signalling pathways.-
dc.languageeng-
dc.publisherElsevier BV. The Journal's web site is located at http://www.elsevier.com/wps/find/journaldescription.cws_home/717426/description#description-
dc.relation.ispartofJournal of Functional Foods-
dc.subjectIcaritin-
dc.subjectCardiac H9c2 cells-
dc.subjectOxidative stress-
dc.subjectNF-E2-related factor 2-
dc.subjectCalcium ion-
dc.titleIcaritin protects against oxidative stress-induced injury in cardiac H9c2 cells via Akt/Nrf2/HO-1 and calcium signalling pathways-
dc.typeArticle-
dc.identifier.emailLeung, GPH: gphleung@hkucc.hku.hk-
dc.identifier.authorityLeung, GPH=rp00234-
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1016/j.jff.2015.06.054-
dc.identifier.scopuseid_2-s2.0-84942510901-
dc.identifier.hkuros297959-
dc.identifier.volume18-
dc.identifier.issuePt. A-
dc.identifier.spage213-
dc.identifier.epage223-
dc.publisher.placeNetherlands-

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