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Comparison of pyrroloquinoline quinone and/or metoprolol on myocardial infarct size and mitochondrial damage in a rat model of ischemia/reperfusion injury.

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The cardioprotective effectiveness of low-dose pyrroloquinoline quinone (PQQ, 3 mg/kg) was compared with metoprolol, a beta(1)-selective adrenoceptor antagonist. Rats underwent 30 minutes of left anterior descending coronary artery occlusion and 2 hours of reperfusion. Metoprolol and/or PQQ were

Pyrroloquinoline quinone (PQQ) decreases myocardial infarct size and improves cardiac function in rat models of ischemia and ischemia/reperfusion.

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As pyrroloquinoline quinone (PQQ) is a redox cofactor in mammals, we asked if it is cardioprotective. Rats were subjected to 2 h of left anterior descending (LAD) coronary artery ligation without reperfusion (model 1, ischemia). In model 2 (ischemia/reperfusion), rats were subjected to 17 or 30 min

Reduction of infarct size by the therapeutic protein TAT-Ndi1 in vivo.

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Lethal myocardial ischemia-reperfusion (I/R) injury has been attributed in part to mitochondrial respiratory dysfunction (including damage to complex I) and the resultant excessive production of reactive oxygen species. Recent evidence has shown that reduced nicotinamide adenine dinucleotide-quinone

The antioxidant enzyme quinone reductase is up-regulated in vivo following cerebral ischemia.

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An astrocyte antioxidant enzyme, quinone reductase (QR), was studied in vivo to assess whether its activity was up-regulated following cerebral ischemia. Rats were given a unilateral focal cerebral infarct and regions of interest within the ischemic penumbra compared to the non-ischemic side for QR

Effect of tacrolimus on myocardial infarction is associated with inflammation, ROS, MAP kinase and Akt pathways in mini-pigs.

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OBJECTIVE This study tested the hypothesis that tacrolimus therapy limited left ventricular (LV) infarct and remodeling by suppressing the inflammatory response, oxidative stress and regulating the mitogen-activated protein kinase (MAPK) and Akt signaling pathways in an acute myocardial infarction

Coenzyme Q10 and antioxidants in acute myocardial infarction.

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Sixty-one patients admitted with acute myocardial infarction, and a symptom's duration of less than 6 hr were randomized into two groups. Immediately after hospitalisation, members of the verum group (n = 32) received 500 mcg of selenium (as sodium selenite). Thereafter they received a daily dosage

Neuroprotection by pyrroloquinoline quinone (PQQ) in reversible middle cerebral artery occlusion in the adult rat.

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Pyrroloquinoline quinone (PQQ) is a naturally occurring redox cofactor that acts as an essential nutrient, antioxidant, and redox modulator. It has previously been reported to reduce infarct size in 7-day-old rat pups with an in vivo cerebral hypoxia/ischemia model (Jensen et al., 1994). In this

The putative essential nutrient pyrroloquinoline quinone is neuroprotective in a rodent model of hypoxic/ischemic brain injury.

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Pyrroloquinoline quinone is a ubiquitous redox cofactor and putative essential nutrient in mammals. Pyrroloquinoline quinone has recently been demonstrated to depress N-methyl-D-asparate induced electrical responses and is neuroprotective in vitro. In addition, pyrroloquinoline quinone has been

Altering pyrroloquinoline quinone nutritional status modulates mitochondrial, lipid, and energy metabolism in rats.

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We have reported that pyrroloquinoline quinone (PQQ) improves reproduction, neonatal development, and mitochondrial function in animals by mechanisms that involve mitochondrial related cell signaling pathways. To extend these observations, the influence of PQQ on energy and lipid relationships and

A new, simple and accurate method for determining ejection fraction by Doppler echocardiography.

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OBJECTIVE To evaluate the feasibility, accuracy and reproducibility of a new and simple method for determining ejection fraction by Doppler echocardiography. This method should theoretically be less influenced by the distortions of left ventricular geometry caused by prior myocardial

Determination of in plasma samples by dual-electrode amperometric detection and liquid chromatography

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Co-Q10 is a lipid-soluble benzoquinone that is an important factor in free radical scavenging, mitochondrial membrane stability and ATP synthesis. Dietary Co-Q10 is a powerful antioxidant that has been useful in lessening the damage associated with ischemia-reperfusion injuries and aiding in the

[Assessment of left ventricular ejection fraction by echocardiography].

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A new simplified echocardiography method to assess left ventricular (LV) ejection fraction (EF), combining routine M-mode and 2-D echo, was used to measure LV size and evaluate regional wall motion. Echocardiography was performed prior to cardiac catheterization in 35 patients aged 38-69 years (mean

Xenotransplantation of mitochondrial electron transfer enzyme, Ndi1, in myocardial reperfusion injury.

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A significant consequence of ischemia/reperfusion (I/R) is mitochondrial respiratory dysfunction, leading to energetic deficits and cellular toxicity from reactive oxygen species (ROS). Mammalian complex I, a NADH-quinone oxidoreductase enzyme, is a multiple subunit enzyme that oxidizes NADH and

Cytotoxicity of major tanshinones isolated from Danshen (Salvia miltiorrhiza) on HepG2 cells in relation to glutathione perturbation.

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Tanshinones are abietane type-diterpene quinones isolated from the roots of Radix Salvia miltiorrhiza (Danshen), a well-known traditional Chinese medicine in the treatment of cardiovascular diseases. Among the major diterpenes isolated, including cryptotanshinone, tanshinone I, tanshinone IIA and

Che-1 attenuates hypoxia/reoxygenation-induced cardiomyocyte apoptosis by upregulation of Nrf2 signaling.

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OBJECTIVE Hypoxia/reoxygenation (H/R)-induced cardiomyocyte apoptosis plays a critical role in the development of myocardial infarction. Che-1 has been reported as an anti-apoptotic gene in response to various cellular stresses. However, whether Che-1 regulates cardiomyocyte apoptosis in myocardial

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