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Conference Paper: Remifentanil preconditioning confers cardioprotection via the JAK/STAT but not PI3K/Akt pathway in rats

TitleRemifentanil preconditioning confers cardioprotection via the JAK/STAT but not PI3K/Akt pathway in rats
Authors
Issue Date2011
PublisherFederation of American Societies for Experimental Biology. The Journal's web site is located at http://www.fasebj.org/
Citation
The 2011 Annual Meeting of Experiment Biology (EB 2011), Washington, DC., 9-13 April 2011. In The FASEB Journal, 2011, v. 25 n. S1, abstract no. 1085.6 How to Cite?
AbstractThe opioid receptor agonist remifentanil (REM) has been shown to attenuate myocardial ischemia reperfusion injury, but the underlying mechanism is unclear. We hypothesized that REM confers cardioprotection by activating the JAK/STAT and PI3K/Akt pathways, two important survival signal pathways for rescuing ischemic myocardium. After anesthesia, male Sprague-Dawley rats were subjected to 30 min of coronary artery occlusion followed by 2 hours of reperfusion. Rats (n=5–6/group) were treated with vehicle, REM preconditioning (6 μg/kg, 3 consecutive 5 min intravenous REM interspersed with 5 min infusion-free periods), or the GSK3β kinase inhibitor SB216763 (SB, 600 μg/kg) immediately prior to inducing ischemia in the absence or concomitant presence of the putative JAK2 inhibitor AG490 (3 mg/kg) or the PI3K inhibitor wortmannin (15 μg/kg). Myocardial infarct size (IS) was significantly reduced by either REM (25±10%) or SB (18±8%) compared to vehicle control (46±13%) (P<0.05). AG490 but not wortmannin abolished the IS sparing effect of REM, although AG490 or wortmannin alone did not significantly affect IS. REM enhanced myocardial phosphorylation of STAT3 and GSK3β compared with that of vehicle-treated rats (P<0.05), and AG490 abolished these effects of REM. By contrast, REM reduced Akt phosphorylation. It is concluded that REM confers cardioprotection via the JAK/STAT but not the PI3K/Akt pathway. Supported by RGC/GRF grant (766709M to MGI) and NSFC grant (30872447 to ZX)
Persistent Identifierhttp://hdl.handle.net/10722/140871
ISSN
2021 Impact Factor: 5.834
2020 SCImago Journal Rankings: 1.709
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorQiao, Sen_US
dc.contributor.authorLiu, Yen_US
dc.contributor.authorWang, Ten_US
dc.contributor.authorMao, Xen_US
dc.contributor.authorWong, GTCen_US
dc.contributor.authorXia, Zen_US
dc.contributor.authorIrwin, MGen_US
dc.date.accessioned2011-09-23T06:20:29Z-
dc.date.available2011-09-23T06:20:29Z-
dc.date.issued2011en_US
dc.identifier.citationThe 2011 Annual Meeting of Experiment Biology (EB 2011), Washington, DC., 9-13 April 2011. In The FASEB Journal, 2011, v. 25 n. S1, abstract no. 1085.6en_US
dc.identifier.issn0892-6638-
dc.identifier.urihttp://hdl.handle.net/10722/140871-
dc.description.abstractThe opioid receptor agonist remifentanil (REM) has been shown to attenuate myocardial ischemia reperfusion injury, but the underlying mechanism is unclear. We hypothesized that REM confers cardioprotection by activating the JAK/STAT and PI3K/Akt pathways, two important survival signal pathways for rescuing ischemic myocardium. After anesthesia, male Sprague-Dawley rats were subjected to 30 min of coronary artery occlusion followed by 2 hours of reperfusion. Rats (n=5–6/group) were treated with vehicle, REM preconditioning (6 μg/kg, 3 consecutive 5 min intravenous REM interspersed with 5 min infusion-free periods), or the GSK3β kinase inhibitor SB216763 (SB, 600 μg/kg) immediately prior to inducing ischemia in the absence or concomitant presence of the putative JAK2 inhibitor AG490 (3 mg/kg) or the PI3K inhibitor wortmannin (15 μg/kg). Myocardial infarct size (IS) was significantly reduced by either REM (25±10%) or SB (18±8%) compared to vehicle control (46±13%) (P<0.05). AG490 but not wortmannin abolished the IS sparing effect of REM, although AG490 or wortmannin alone did not significantly affect IS. REM enhanced myocardial phosphorylation of STAT3 and GSK3β compared with that of vehicle-treated rats (P<0.05), and AG490 abolished these effects of REM. By contrast, REM reduced Akt phosphorylation. It is concluded that REM confers cardioprotection via the JAK/STAT but not the PI3K/Akt pathway. Supported by RGC/GRF grant (766709M to MGI) and NSFC grant (30872447 to ZX)-
dc.languageengen_US
dc.publisherFederation of American Societies for Experimental Biology. The Journal's web site is located at http://www.fasebj.org/-
dc.relation.ispartofThe FASEB Journalen_US
dc.titleRemifentanil preconditioning confers cardioprotection via the JAK/STAT but not PI3K/Akt pathway in ratsen_US
dc.typeConference_Paperen_US
dc.identifier.emailQiao, S: qiao1983@hku.hken_US
dc.identifier.emailWang, T: wangtt6@hku.hken_US
dc.identifier.emailWong, GTC: gordon@hku.hken_US
dc.identifier.emailXia, Z: zyxia@hku.hken_US
dc.identifier.emailIrwin, MG: mgirwin@hku.hken_US
dc.identifier.authorityWong, GTC=rp00523en_US
dc.identifier.authorityXia, Z=rp00532en_US
dc.identifier.authorityIrwin, MG=rp00390en_US
dc.description.natureabstract-
dc.identifier.doi10.1096/fasebj.25.1_supplement.1085.6-
dc.identifier.hkuros193522en_US
dc.identifier.volume25en_US
dc.identifier.issueS1-
dc.identifier.spageabstract no. 1085.6-
dc.identifier.epageabstract no. 1085.6-
dc.identifier.isiWOS:000310708401140-
dc.identifier.issnl0892-6638-

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