Second window of ischemic preconditioning regulates mitochondrial permeability transition pore by enhancing Bcl-2 expression

Katare, Rajesh; Sasaguri, Shiro; Zhitian, Zou; Suzuki, Ryoko; Asakai, Rei; Maeda, Hironori

doi:10.1016/s0008-6363(03)00358-4

Cited by 61 publications

(47 citation statements)

References 28 publications

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“…The magnitude of immediate protection afforded by Gd in the current study is less than the protection reported with ischemic preconditioning (31% vs. 86% reduction in infarct size) (11), but the fact that Gd can be given one minute before reperfusion and still provide significant infarct reduction makes it perhaps more clinically important than ischemic preconditioning. In addition to these temporal relationships, we observed that a single dose of Gd confers delayed cardioprotection for up to 72 hours to an extent that is comparable to delayed cardioprotection observed with ischemic preconditioning (66% vs. 67% reduction in infarct size) (12). This effect may also have important clinical applications in revascularization procedures, where recurrent ischemia may occur early after the procedure from graft occlusion or PCI failure.…”

Section: Discussionsupporting

confidence: 58%

Gadolinium limits myocardial infarction in the rat: Dose–response, temporal relations and mechanisms

Nicolosi

Strande

Hsu

et al. 2008

Journal of Molecular and Cellular Cardiology

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The lanthanide cation, gadolinium (Gd) attenuates post-ischemic myocardial stunning. This study tests the hypothesis that Gd also preconditions the myocardium against infarction following ischemia-reperfusion (IR), and explores potential mechanisms underlying Gd-induced cardioprotection. Regional myocardial infarction was induced in rats by occluding the left anterior descending artery for 30 minutes and reperfusing for 120 minutes. Rats (n = 6/group) were administered intravenous Gd (1 to 100 μmol/kg) 15 minutes prior to ischemia. Hearts were excised after reperfusion to determine infarct size (IS) and area at risk (AAR). The ratio IS/AAR (%) was reduced by Gd in a "U"-shaped, dose-dependent manner. The minimum dose that reduced IS/AAR was 5 μmol/kg (52 ± 5% vs. 64 ± 4%), while the dose that reduced IS/AAR maximally was 20 μmol/ kg (44 ± 4%). Gd also reduced IS/AAR when given 1 minute before reperfusion (47 ± 3%) but not when given 10 seconds after reperfusion (60 ± 3%). Cardioprotection was maintained if I-R was delayed 24-72 hours after Gd administration. Cardioprotection by Gd was abolished by inhibition of JAK-2 with AG-490, of p42/44 MAPK with PD98059 or of K ATP channels with glibenclamide.

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Section: Discussionsupporting

confidence: 58%

Gadolinium limits myocardial infarction in the rat: Dose–response, temporal relations and mechanisms

Nicolosi

Strande

Hsu

et al. 2008

Journal of Molecular and Cellular Cardiology

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“…Accordingly, the goals of the present study were to determine whether pretreatment with nicorandil, in the absence of ischemia, can reproduce the protective effect of the late phase of ischemic PC against myocardial infarction and to determine whether nicorandil-induced delayed cardioprotection is associated with expression of COX-2 and Bcl-2, which has previously been shown to increase 24 h after ischemic PC (51,59). All studies were performed in our well-established conscious rabbit model (51,59).…”

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confidence: 99%

Nicorandil induces late preconditioning against myocardial infarction in conscious rabbits

Tang

Xuan

Zhu

et al. 2004

American Journal of Physiology-Heart and Circulatory Physiology

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Nicorandil has been shown to induce an infarct-limiting effect similar to that induced by the early phase of ischemic preconditioning (PC). The goals of this study were to determine whether nicorandil induces a delayed cardioprotection that is analogous to the late phase of ischemic PC and, if so, whether nicorandil-induced late PC is associated with upregulation of cardioprotective proteins. Chronically instrumented, conscious rabbits received vehicle (intravenous normal saline; control group, n = 10), nicorandil (100 μg/kg bolus + 30 μg·kg–1·min–1 iv for 60 min; nicorandil group, n = 10), or ischemic PC (6 cycles of 4-min coronary occlusion/4-min reperfusion; PC group, n = 8). Twenty-four hours later, rabbits underwent a 30-min coronary occlusion, followed by 3 days of reperfusion. Myocardial infarct size was significantly reduced in rabbits pretreated with nicorandil (27.5 ± 5.3% of the risk region) or with ischemia (30.3 ± 4.2%) versus controls (59.1 ± 4.7%, P < 0.05 vs. both). Furthermore, the expression of cyclooxygenase-2 (COX-2) and Bcl-2 was significantly elevated (+38% and +126%, respectively; P < 0.05) in myocardium of rabbits given nicorandil 24 h earlier versus controls. We conclude that nicorandil induces delayed cardioprotection against myocardial infarction similar to that afforded by the late phase of ischemic PC, possibly by upregulating COX-2 and Bcl-2.

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“…The other possible reason could be that the mild stress in the form of food restriction and exercise, before cardiac ischemia and failure, conditions the myocardium against the formation of free radicals at a later date. This is similar to the protective effects of ischemic preconditioning, where mild ischemia before the prolonged ischemia can protect the myocardium from severe ischemic damage (21,22). Calorie restriction (CR) or food restriction (FR) must be considered separately from food starvation and defined as a reduction in calorie or food intake below the usual ad libitum intake without malnutrition.…”

Section: Discussionmentioning

confidence: 99%

Regular Exercise or Food Restriction, Which is Better in the Event of Heart Failure? An Approach to Oxidative Stress and Angiogenesis

Moradi

Imani

Shakoori

et al. 2016

Ann. Appl. Sport Sci

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The aim of present study was to investigate whether food restriction combined with exercise training could attenuate the oxidative stress and promote angiogenesis in a rat model of heart failure. 50 male wistar rats weighing 250-300 g were randomly divided into 5 groups including: 1) sham; they were fed ad libitum food, n=10. 2) Heart failure group; 3) Exercise group; they run on a treadmill 5 days per week for 4 weeks, n=10. 4) Food restricted group; they were fed with 60% of their daily average food intake, n=10. 5) Food restricted plus exercise group; as well as feeding with 60% of their daily average food intake for 8 weeks and run on a treadmill 5 days for the 4 next weeks, n=10. Subcutaneous injection of isoproterenol (130 mg/kg) was used to induce experimental heart failure. Echocardiographic parameters were monitored. Plasma levels of malondialdehyde (MDA) and prooxidant/ antioxidant balance (PAB), as oxidative parameters were measured. In continue gene expression of angiogenic factors such as hypoxia inducible factor-1a (HIF-1a), vascular endothelial growth factor A (VEGFA) and endothelial nitric oxide synthase (eNOS) as well as histopathological examination were investigated. Isoproterenol-treated hearts showed lower functional indexes including LVEDd; Left Ventricular End Diastolic dimension (p<0.05), FS; Fractional Shortening (p<0.001), EF; Ejection Fraction, (p<0.001). In addition, significant increase in plasma levels of MDA (p<0.001) and PAB (p<0.001) were observed. Food restriction and exercise significantly improved all measured parameters. The protective role of food restriction and exercise training on myocardial damage was further confirmed by promoting the gene expression of angiogenic factors (p<0.001) in left ventricle and reducing the myocardial fibrosis (p<0.05). Our results suggest that combined food restriction with exercise training is superior to either therapy alone for improving functional indexes, strengthen balance of antioxidative defense system, as well as gene expression of angiogenic factors and decreasing myocardial fibrosis.

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Second window of ischemic preconditioning regulates mitochondrial permeability transition pore by enhancing Bcl-2 expression

Abstract: The cytoprotective effects of SWOP are dependent on PTP activation state and may involve upregulation of Bcl-2 expression.

Cited by 61 publications

References 28 publications

Gadolinium limits myocardial infarction in the rat: Dose–response, temporal relations and mechanisms

Gadolinium limits myocardial infarction in the rat: Dose–response, temporal relations and mechanisms

Nicorandil induces late preconditioning against myocardial infarction in conscious rabbits

Regular Exercise or Food Restriction, Which is Better in the Event of Heart Failure? An Approach to Oxidative Stress and Angiogenesis

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