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cytochrome c/blödning
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Cytochrome c limits oxidative stress and decreases acidosis in a rat model of hemorrhagic shock and reperfusion injury.
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Hemorrhagic shock and reperfusion (HSR) injury leads to a cascade of reactive oxygen species (ROS) production and mitochondrial dysfunction, which results in energy failure, cell death, and multiple organ dysfunction. Cytochrome c (cyt c) is the final electron carrier in the mitochondrial electron
[Effects of Nao-Yi-An granule on activity of cytochrome c oxidase in hippocampus of experimental intracerebral hemorrhagic rats].
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OBJECTIVE
To explore the neuronal protective effects of a traditional Chinese medicine complex Nao-Yi-An granule(NYA) on experimental intracerebral hemorrhage(ICH) in rats.
METHODS
Eighty collagenase-induced ICH rats were used. At 12 h, 24 h, 2 d, 4 d, 7 d, cytochrome c oxidase(CO) activity was
[Use water-soluble and lipid-bound forms of cytochrome C for the treatment of experimental hemorrhagic shock].
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[Action of cytochrome C in hemorrhages].
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[Cytochrome C in post-hemorrhagic renal lesions].
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[Use of cytochrome "C" in treating acute massive hemorrhage].
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Carnosine Attenuates Brain Oxidative Stress and Apoptosis After Intracerebral Hemorrhage in Rats.
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Carnosine, an endogenous dipeptide (β-alanyl-L-histidine), exerts multiple neuroprotective properties, but its role in intracerebral hemorrhage (ICH) remains unclear. This study investigates the effect of Carnosine on brain injury using the rat ICH model, which is established by type IV collagenase
SS31 attenuates oxidative stress and neuronal apoptosis in early brain injury following subarachnoid hemorrhage possibly by the mitochondrial pathway.
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Effect of estrogen on mitochondrial function and intracellular stress markers in rat liver and kidney following trauma-hemorrhagic shock and prolonged hypotension.
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Trauma-hemorrhage (T-H) is known to impair tissue perfusion, leading to tissue hypoxia, and thus affecting mitochondria, the organelles with the highest oxygen demand. In a model of T-H and prolonged hypotension without fluid resuscitation, administration of a small volume of 17beta-estradiol (E2),
Both endoplasmic reticulum and mitochondrial pathways are involved in oligodendrocyte apoptosis induced by capsular hemorrhage.
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OBJECTIVE
The white matter injury caused by intracerebral hemorrhage (ICH) includes demyelination and axonal injury. Oligodendrocyte apoptosis is reported to be involved in triggering demyelination. Experimental observations indicate that both endoplasmic reticulum and mitochondrial pathways could
Heme oxygenase 2 deficiency increases brain swelling and inflammation after intracerebral hemorrhage.
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Intracerebral hemorrhage (ICH) remains a major medical problem and currently has no effective treatment. Hemorrhaged blood is highly toxic to the brain, and catabolism of the pro-oxidant heme, mainly released from hemoglobin, is critical for the resolution of hematoma after ICH. The degradation of
Administration of glutamine after hemorrhagic shock restores cellular energy, reduces cell apoptosis and damage, and increases survival.
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BACKGROUND
Hemorrhagic shock causes a rapid depletion of adenosine triphosphate (ATP) and an increase of the terminal metabolite xanthine. Free radicals generated from xanthine oxidase play a major role in cell injury. Programmed cell death, apoptosis, is a major pathway causing reperfusion injury.
The development of an improved preclinical mouse model of intracerebral hemorrhage using double infusion of autologous whole blood.
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The present study was conducted in mice to validate a double blood infusion model of intracerebral hemorrhage (ICH) that does not use anticoagulant. We investigated the effect of intrastriatal infusion of blood on hematoma volume, neurologic function, brain edema and swelling, and markers of
RECOMBINANT BCL-XL ATTENUATES VASCULAR HYPERPERMEABILITY IN A RAT MODEL OF HEMORRHAGIC SHOCK.
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Following hemorrhagic shock (HS), vascular hyperpermeability i.e. the leakage of fluid, nutrients and proteins into the extravascular space occurs primarily due to the disruption of the endothelial cell-cell adherens junctional complex. Studies from our laboratory demonstrate that activation of the
Nuclear receptor nur77 promotes cerebral cell apoptosis and induces early brain injury after experimental subarachnoid hemorrhage in rats.
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Nur77 is a potent proapoptotic member of the nuclear receptor superfamily that is expressed predominantly in brain tissue. It has been demonstrated that Nur77 mediates apoptosis in multiple organs. Nur77-mediated early brain injury (EBI) involves a conformational change in BCL-2 and triggers
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