Mitochondrial function in response to cardiac ischemia-reperfusion after oral treatment with quercetin

Brookes, Paul S.; Digerness, Stanley B.; Parks, Dale A.; Darley‐Usmar, Victor

doi:10.1016/s0891-5849(02)00839-0

Cited by 84 publications

(48 citation statements)

References 46 publications

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“…from 0.033 mg/kg (Brookes et al, 2002) to 100 mg/kg (Guzy et al, 2003) and even 800 mg/kg per day (de Boer et al, 2005). Surprisingly, despite a 3,000-fold difference of the amount of quercetin administered (i.e.…”

Section: Discussionmentioning

confidence: 99%

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The effect of crataegus fruit extract and some of its flavonoids on mitochondrial oxidative phosphorylation in the heart

Bernatonienė

Trumbeckaitė

Majienė

et al. 2009

Phytotherapy Research

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To cite this version:Jurga Bernatoniene, Sonata Trumbeckaite, Daiva Majiene, Rasa Baniene, Giedre Baliutyte, et al.. The effect of Crataegus fruit extract and some of its flavonoids on mitochondrial oxidative phosphorylation in the heart. Phytotherapy Research, Wiley, 2009, 23 (12) ng/ml to 13.9 µg/ml of Crataegus phenolic compounds (PC)) and its several pure flavonoids on isolated rat heart mitochondria respiring on pyruvate+malate, succinate and palmitoyl-L-carnitine+malate. CE at doses under 278 ng/ml of PC had no effect on mitochondrial functions. At concentrations from 278 ng/ml to 13.9 µg/ml of PC, CE

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Section: Discussionmentioning

confidence: 99%

“…This issue is complicated due to several circumstances. It is known (Brookes et al, 2002) that polyphenols, after intake, undergo various conversions, but the effects of most metabolites on mitochondria are not known.…”

Section: Discussionmentioning

confidence: 99%

The effect of crataegus fruit extract and some of its flavonoids on mitochondrial oxidative phosphorylation in the heart

Bernatonienė

Trumbeckaitė

Majienė

et al. 2009

Phytotherapy Research

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“…Flavonoids inhibit many enzymes, including cyclooxygenase, lipoxygenase (2, 52), phospholipase A 2 (2), and STAT-1 activation (68). Flavonoids also act as antioxidants (11,14) and have anti-inflammatory actions (26). The specific actions of flavones may have been to increase the binding affinity of substrate (39) or to improve the electron transfer efficiency between NADPH/ cytochrome P-450 reductase and the P-450 enzyme (37,45).…”

Section: Discussionmentioning

confidence: 99%

Cardioprotective mechanisms ofPrunus cerasus(sour cherry) seed extract against ischemia-reperfusion-induced damage in isolated rat hearts

Bak¹,

Lekli²,

Juhász³

et al. 2006

American Journal of Physiology-Heart and Circulatory Physiology

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Cardioprotective mechanisms of Prunus cerasus (sour cherry) seed extract against ischemia-reperfusion-induced damage in isolated rat hearts. Am J Physiol Heart Circ Physiol 291: H1329 -H1336, 2006. First published April 14, 2006 doi:10.1152/ajpheart.01243.2005The effects of kernel extract obtained from sour cherry (Prunus cerasus) seed on the postischemic cardiac recovery were studied in isolated working rat hearts. Rats were treated with various daily doses of the extract for 14 days, and hearts were then isolated and subjected to 30 min of global ischemia followed by 120 min of reperfusion. The incidence of ventricular fibrillation (VF) and tachycardia (VT) fell from their control values of 92% and 100% to 50% (not significant) and 58% (not significant), 17% (P Ͻ 0.05), and 25% (P Ͻ 0.05) with the doses of 10 mg/kg and 30 mg/kg of the extract, respectively. Lower concentrations of the extract (1 and 5 mg/kg) failed to significantly reduce the incidence of VF and VT during reperfusion. Sour cherry seed kernel extract (10 and 30 mg/kg) significantly improved the postischemic recovery of cardiac function (coronary flow, aortic flow, and left ventricular developed pressure) during reperfusion. We have also demonstrated that the extract-induced protection in cardiac function significantly reflected in a reduction of infarct size. Immunohistochemistry indicates that a reduction in caspase-3 activity and apoptotic cells by the extract, beside other potential action mechanisms of proanthocyanidin, trans-resveratrol, and flavonoid components of the extract, could be responsible for the cardioprotection in ischemic-reperfused myocardium.

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“…Assessing mitochondrial function in this system is important, because it correlates closely with cardiac contractility after IR injury [44]; whereas it is not immediately apparent that cardiomyocyte viability necessarily translates to changes in contractility at the whole heart level. Therefore Δ ψm , a commonly used mitochondrial functional parameter, was measured and the results (Figure 3) show that HR injury significantly depleted Δ ψm .…”

Section: Protection Of Cardiomyocytes Against Hr Injury By Gsno and Smentioning

confidence: 99%

Cardioprotection and mitochondrial S-nitrosation: Effects of S-nitroso-2-mercaptopropionyl glycine (SNO-MPG) in cardiac ischemia–reperfusion injury

Nadtochiy

Burwell

Brookes

2007

Journal of Molecular and Cellular Cardiology

131

116

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Mitochondrial dysfunction is a key pathologic event in cardiac ischemia-reperfusion (IR) injury, and protection of mitochondrial function is a potential mechanism underlying ischemic preconditioning (IPC). Acknowledging the role of nitric oxide (NO • ) in IPC, it was hypothesized that mitochondrial protein S-nitrosation may be a cardioprotective mechanism. The reagent S-nitroso-2-mercaptopropionyl-glycine (SNO-MPG) was therefore developed to enhance mitochondrial Snitrosation and elicit cardioprotection. Within cardiomyocytes, mitochondrial proteins were effectively S-nitrosated by SNO-MPG. Consistent with the recent discovery of mitochondrial complex I as an S-nitrosation target, SNO-MPG inhibited complex I activity and cardiomyocyte respiration. The latter effect was insensitive to the NO • scavenger c-PTIO, indicating no role for NO • -mediated complex IV inhibition. A cardioprotective role for reversible complex I inhibition has been proposed, and consistent with this SNO-MPG protected cardiomyocytes from simulated IR injury. Further supporting a cardioprotective role for endogenous mitochondrial S-nitrosothiols, patterns of protein S-nitrosation were similar in mitochondria isolated from Langendorff perfused hearts subjected to IPC, and mitochondria or cells treated with SNO-MPG. The functional recovery of perfused hearts from IR injury was also improved under conditions which stabilized endogenous S-nitrosothiols (i.e. dark), or by pre-ischemic administration of SNO-MPG. Mitochondria isolated from SNO-MPG-treated hearts at the end of ischemia exhibited improved Ca 2+ handling and lower ROS generation. Overall these data suggest that mitochondrial S-nitrosation and complex I inhibition constitute a protective signaling pathway that is amenable to pharmacologic augmentation.

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Mitochondrial function in response to cardiac ischemia-reperfusion after oral treatment with quercetin

Cited by 84 publications

References 46 publications

The effect of crataegus fruit extract and some of its flavonoids on mitochondrial oxidative phosphorylation in the heart

The effect of crataegus fruit extract and some of its flavonoids on mitochondrial oxidative phosphorylation in the heart

Cardioprotective mechanisms ofPrunus cerasus(sour cherry) seed extract against ischemia-reperfusion-induced damage in isolated rat hearts

Cardioprotection and mitochondrial S-nitrosation: Effects of S-nitroso-2-mercaptopropionyl glycine (SNO-MPG) in cardiac ischemia–reperfusion injury

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