rotenone/infarkt

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Endothelin-1 production is enhanced by rotenone, a mitochondrial complex I inhibitor, in cultured rat cardiomyocytes.

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In chronic heart failure and acute myocardial infarction, the tissue level of endothelin (ET)-1 in the heart, as well as its plasma level, has been reported to increase markedly. There is, however, little information about what in these pathologic conditions leads to increased production of ET-1,

Rotenone decreases ischemia-induced injury by inhibiting mitochondrial permeability transition in mature brains.

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The mitochondrial permeability transition pore (mPTP) is thought to be implicated in brain ischemia-induced cell death. Here we sought to determine whether complex I (CI) of the mitochondrial electron transfer system may be involved in regulation of mPTP opening during ischemia and whether a

Reactive oxygen species generated by mitochondrial injury in human brain microvessel endothelial cells.

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Generation of reactive oxygen species (ROS) and their detrimental effects on the brain after transient ischemia are widely recognized. We studied ROS production from mitochondria in human brain microvessel endothelial cells (HBEC) under chemical hypoxia. HBEC in confluent conditions were incubated

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

Total synthesis and cytoprotective properties of dykellic acid.

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Small molecule inhibitors of apoptosis hold considerable promise for the treatment of a host of diseases, including neurodegeneration, myocardial infarction, and stroke. Many compounds that delay or prevent apoptotic death either reduce the amount of cellular reactive oxygen species (ROS) or are

Uridine-5'-triphosphate (UTP) maintains cardiac mitochondrial function following chemical and hypoxic stress.

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Previously we found that uridine-5'-triphosphate (UTP) significantly decreased cultured cardiomyocyte death, induced by hypoxia via activating P2Y(2) receptors, reduced infarct size and maintained higher ATP levels in an in vivo model. Mitochondrial contribution to the progression of cardiomyocyte

Detection of ischemic neuronal damage with [¹⁸F]BMS-747158-02, a mitochondrial complex-1 positron emission tomography ligand: small animal PET study in rat brain.

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The acute and subacute ischemic neuronal damage in rat brain caused by photochemically induced thrombosis (PIT) was imaged using [¹⁸F]BMS-747158-02 ([¹⁸F]BMS) for mitochondrial complex-1 (MC-1) and [¹¹C](R)-PK11195 ([¹¹C](R)-PK) for peripheral benzodiazepine receptor [PBR; translocator protein] at

Mitochondrial Impairment in Cerebrovascular Endothelial Cells is Involved in the Correlation between Body Temperature and Stroke Severity.

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Stroke is the second leading cause of death worldwide. The prognostic influence of body temperature on acute stroke in patients has been recently reported; however, hypothermia has confounded experimental results in animal stroke models. This work aimed to investigate how body temperature could

Ischemic preconditioning does not protect via blockade of electron transport.

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Ischemic preconditioning (IPC) before sustained ischemia decreases myocardial infarct size mediated in part via protection of cardiac mitochondria. Reversible blockade of electron transport at complex I immediately before sustained ischemia also preserves mitochondrial respiration and decreases

Characterization of autoantigenic sites on isolated dog heart mitochondria.

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1. Anti-heart mitochondria autoantibodies were developed in serum from dogs following experimental myocardial infarction. 2. Heart mitochondria frozen and thawed repeatedly in a sucrose/Tris-chloride buffer retained both their functional integrity as measured by the respiratory control ratio and

Acrolein activates matrix metalloproteinases by increasing reactive oxygen species in macrophages.

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Acrolein is a ubiquitous component of environmental pollutants such as automobile exhaust, cigarette, wood, and coal smoke. It is also a natural constituent of several foods and is generated endogenously during inflammation or oxidation of unsaturated lipids. Because increased inflammation and

PEGylated Erythropoietin Protects against Brain Injury in the MCAO-Induced Stroke Model by Blocking NF-κB Activation.

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Cerebral ischemia exhibits a multiplicity of pathophysiological mechanisms. During ischemic stroke, the reactive oxygen species (ROS) concentration rises to a peak during reperfusion, possibly underlying neuronal death. Recombinant human erythropoietin (EPO) supplementation is one method of treating

Synthesis and preliminary evaluation of 18F-labeled pyridaben analogues for myocardial perfusion imaging with PET.

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In this study the (18)F-labeled pyridaben analogs 2-tertbutyl-4-chloro-5-(4-(2-(18)F-fluoroethoxy))benzyloxy-2H-pyridazin-3-one ((18)F-FP1OP) and 2-tertbutyl-4-chloro-5-(4-(2-(2-(2-(18)F-fluoroethoxy)ethoxy)ethoxy))benzyloxy-2H-pyridazin-3-one ((18)F-FP3OP) were synthesized, characterized, and

Isoflurane differentially modulates mitochondrial reactive oxygen species production via forward versus reverse electron transport flow: implications for preconditioning.

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BACKGROUND Reactive oxygen species (ROS) mediate the effects of anesthetic precondition to protect against ischemia and reperfusion injury, but the mechanisms of ROS generation remain unclear. In this study, the authors investigated if mitochondria-targeted antioxidant (mitotempol) abolishes the

Neuroprotective effect of a new DJ-1-binding compound against neurodegeneration in Parkinson's disease and stroke model rats.

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BACKGROUND Parkinson's disease (PD) and cerebral ischemia are chronic and acute neurodegenerative diseases, respectively, and onsets of these diseases are thought to be induced at least by oxidative stress. PD is caused by decreased dopamine levels in the substantia nigra and striatum, and cerebral

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