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Possible mechanism of rottlerin induced modulation of ischemia reperfusion injury in isolated rat hearts.
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The present study was designed to investigate the modulatory effects of rottlerin on ischemia reperfusion induced myocardial injury. Isolated rat hearts were exposed to 30 min of global ischemia followed by 120 min of reperfusion using Langendorff apparatus. Myocardial injury was assessed in the
The infarct size-limiting effect of ischemic postconditioning (IPOC) is suppressed in isolated hyperhomocysteinemic (Hhcy) rat hearts: the reasonable role of PKC-delta.
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BACKGROUND
Recently we have demonstrated that the cardioprotective potential of ischemic postconditioning (IPOC) against ischemia and reperfusion (I/R)-induced myocardial injury was markedly suppressed in hyperhomocysteinemic (Hhcy) rat hearts. The present study investigated the possible role of
Infarct-sparing effect of myocardial postconditioning is dependent on protein kinase C signalling.
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OBJECTIVE
Using non-selective and selective protein kinase C (PKC) epsilon and delta isoform inhibitors, we tested the hypothesis that the cardioprotective phenotype invoked by postconditioning (postcon) is dependent on PKC signalling. Furthermore, we determined whether postconditioning alters
PKC-delta inhibition does not block preconditioning-induced preservation in mitochondrial ATP synthesis and infarct size reduction in rats.
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We have previously demonstrated that cardioprotection induced by the infusion of a selective delta1-opioid agonist is mediated by the specific translocation of PKC-delta to the mitochondria in in vivo rat hearts and via opening of the mitochondrial KATP channel. Ischemic preconditioning (IPC) is
Role of protein kinase Cdelta in endothelin-induced type I collagen expression in cardiac myofibroblasts isolated from the site of myocardial infarction.
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The role of endothelin-1 (ET) in tissue remodeling/fibrogenesis has been demonstrated in various in vitro and in vivo models. Our previous studies have revealed ET-induced expression of type I collagen in cardiac myofibroblasts (myoFb). Here we report that protein kinase Cdelta (PKCdelta) and
The Combination of Astragalus membranaceus and Ligustrazine Protects Against Thrombolysis-Induced Hemorrhagic Transformation Through PKCδ/Marcks Pathway in Cerebral Ischemia Rats
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Astragalus membranaceus (Ast) and ligustrazine (Lig) have a protective effect on lower hemorrhagic transformation induced by pharmaceutical thrombolysis. The cerebral ischemia rat model was induced with autologous blood clot injections. A combination of Ast and Lig, or a protein kinase C
Protein kinase C activation stimulates mesenchymal stem cell adhesion through activation of focal adhesion kinase.
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Emerging evidence suggests that cell therapy with mesenchymal stem cells (MSCs) has beneficial effects on the injured heart. However, the decreased survival and/or adhesion of MSCs under ischemic conditions limits the application of cell transplantation as a therapeutic modality. We investigated a
Possible involvement of PKC-delta in the abrogated cardioprotective potential of ischemic preconditioning in hyperhomocysteinemic rat hearts.
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The present study has been designed to investigate the possible role of protein kinase C-delta (PKC-delta) in hyperhomocysteinemia-induced attenuation of cardioprotective potential of ischemic preconditioning (IPC). Rats were administered L-methionine (1.7 g/kg/day, p.o.) for 4 weeks to produce
Protein kinase C-delta mediates adenosine A3 receptor-induced delayed cardioprotection in mouse.
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We investigated the role of protein kinase C in adenosine A3 receptor (A3AR)-induced delayed cardioprotection in the mouse heart. Mice were treated with selective A3AR agonist N6-(3-iodobenzyl)adenosine-5'-N-methyluronamide (IB-MECA). Twenty-four hours later, hearts were perfused in the Langendorff
Adenosine A(1) receptor mediates late preconditioning via activation of PKC-delta signaling pathway.
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Protein kinase C (PKC) plays a central role in both early and late preconditioning (PC) but its association with inducible nitric oxide synthase (iNOS) is not clear in late PC. This study investigates the PKC signaling pathway in the late PC induced by activation of adenosine A(1) receptor (A(1)R)
Cardioprotection following adenosine kinase inhibition in rat hearts.
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Adenosine kinase phosphorylates adenosine to AMP, the primary pathway for adenosine metabolism under basal conditions. Inhibition of adenosine kinase results in a site-specific increase in interstitial adenosine. Using a rat model of myocardial infarction, we examined the protective effects of
Delta-opioid receptor activation before ischemia reduces gap junction permeability in ischemic myocardium by PKC-epsilon-mediated phosphorylation of connexin 43.
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The aim of this study was to examine the hypothesis that delta-opioid receptor activation before ischemia suppresses gap junction (GJ) permeability by PKC-mediated connexin 43 (Cx43) modulation, which contributes to infarct size limitation afforded by the delta-opioid receptor activation. A
Essential activation of PKC-delta in opioid-initiated cardioprotection.
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Stimulation of the delta(1)-opioid receptor confers cardioprotection to the ischemic myocardium. We examined the role of protein kinase C (PKC) after delta-opioid receptor stimulation with TAN-67 or D-Ala(2)-D-Leu(5)-enkephalin (DADLE) in a rat model of myocardial infarction induced by a 30-min
Increased expression and altered subcellular distribution of PKC-delta in chronically hypoxic rat myocardium: involvement in cardioprotection.
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We examined the role of protein kinase C (PKC) in the cardioprotective mechanism induced by long-term adaptation to chronic intermittent hypoxia. Adult male Wistar rats were exposed to hypobaric hypoxia of 7,000 m for 8 h/day, 5 days/wk; the total number of exposures was 24-32. A control group was
Protein kinase C translocation and Src protein tyrosine kinase activation mediate isoflurane-induced preconditioning in vivo: potential downstream targets of mitochondrial adenosine triphosphate-sensitive potassium channels and reactive oxygen species.
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BACKGROUND
The authors tested the hypotheses that protein kinase C (PKC)-specific isoform translocation and Src protein tyrosine kinase (PTK) activation play important roles in isoflurane-induced preconditioning in vivo.
METHODS
Rats (n = 125) instrumented for measurement of hemodynamics underwent
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