ethyl pyruvate/heilablóðfall

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The effect of ethyl pyruvate and N-acetylcysteine on ischemia-reperfusion injury in an experimental model of ischemic stroke.

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BACKGROUND Reperfusion therapies play an important role in early-period treatment for patients presenting to the emergency department due to stroke. However, the ischemia-reperfusion injury that may occur with reperfusion must then be considered. The purpose of this study was to determine the

Effects of ethyl pyruvate and other α-keto carboxylic acid derivatives in a rat model of multivisceral ischemia and reperfusion.

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BACKGROUND Ethyl pyruvate (EP) has been shown to ameliorate hepatic, renal, and intestinal mucosal injury and down-regulate expression of several pro-inflammatory mediators in a wide variety of preclinical models of critical illnesses, such as sepsis, burn injury, acute pancreatitis, stroke, and

Ethyl pyruvate: a novel anti-inflammatory agent.

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Ethyl pyruvate (EP) is a simple derivative of the endogenous metabolite, pyruvic acid. Treatment with EP has been shown to improve survival and/or ameliorate organ dysfunction in a wide variety of preclinical models of critical illnesses, such as severe sepsis, acute respiratory distress syndrome,

The biochemical basis for the anti-inflammatory and cytoprotective actions of ethyl pyruvate and related compounds.

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Pyruvate is an important metabolic intermediate, and also is an effective scavenger of hydrogen peroxide and other reactive oxygen species (ROS). Pharmacological administration of pyruvate has been shown to improve organ function in animal models of oxidant-mediated cellular injury. However,

Ethyl pyruvate.

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OBJECTIVE Ethyl pyruvate is a simple derivative of the endogenous metabolite, pyruvic acid. Ethyl pyruvate was shown to ameliorate some of the structural and functional changes associated with mesenteric ischemia and reperfusion in rats. RESULTS Treatment with ethyl pyruvate has been shown to

HMGB1 promoted P-glycoprotein at the blood-brain barrier in MCAO rats via TLR4/NF-κB signaling pathway.

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P-glycoprotein (P-gp) is located on the luminal surface of brain vascular endothelium and its status may determine the delivery of the agents into the brain tissues. Previous study showed that upregulation of P-gp at the blood-brain barrier (BBB) after ischemic stroke were mediated by nuclear

Role of HMGB1 in propofol protection of rat intestinal epithelial cells injured by heat shock.

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Gut-derived endotoxin and pathogenic bacteria may be important causative factors of morbidity and death during heat stroke. However, as the key component of intestinal mucosal barrier, the molecular mechanism of how intestinal epithelial cells are injured by heat shock is remains unclear. After rat

HMGB1 promotes neurovascular remodeling via Rage in the late phase of subarachnoid hemorrhage.

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High-mobility group box1 (HMGB1) is a nuclear protein widely expressed in the central nervous system. Extracellular HMGB1 serves as a proinflammatory cytokine and contributes to brain injury during the acute stage post-stroke. Recently, increasing evidence has demonstrated beneficial effects of

HMGB1 may act via RAGE to promote angiogenesis in the later phase after intracerebral hemorrhage.

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Following intracerebral hemorrhage (ICH), high-mobility group box 1 protein (HMGB1) may promote vascular remodeling. Whether HMGB1 supports angiogenesis after ICH is unclear, as are the receptors and downstream signaling pathway(s) involved. We used the rat model of collagenase-induced ICH to

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