propyl gallate/hypoxia

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n-Propyl gallate activates hypoxia-inducible factor 1 by modulating intracellular oxygen-sensing systems.

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HIF-1 (hypoxia-inducible factor 1) is a master regulator of cellular adaptive responses to hypoxia. The expression and transcriptional activity of the HIF-1alpha subunit is stringently controlled by intracellular oxygen tension through the action of prolyl and asparaginyl hydroxylases. In the

Effects of n-propyl gallate on neuronal survival after forebrain ischemia in rats.

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OBJECTIVE The present study was conducted to assess the effects of intraperitoneal administration of n-propyl gallate (PG) on hippocampal neuronal survival after forebrain ischemia. METHODS Forty male Sprague-Dawley rats were randomly assigned to one of 6 groups. Animals in the PG-I-10, PG-I-8 and

Effect of antioxidants on hypoxia/reoxygenation-induced injury in isolated perfused rat liver.

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Isolated perfused livers from rats fasted overnight were subjected to 30 min. of hypoxia followed by reoxygenation for 60 min., resulting in marked cytotoxicity as evidenced by an enhanced release of cytosolic enzymes (lactate dehydrogenase: 14-fold over controls, glutamate-pyruvate-transaminase:

Gallate, the component of HIF-inducing catechins, inhibits HIF prolyl hydroxylase.

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Catechins have recently been reported to increase the cellular content of the hypoxia-inducible factor (HIF)-1alpha within mammalian cells. These catechins have a gallate moiety as a common structure. We now report that n-propyl gallate (nPG) also increases the HIF-1alpha protein in the rat

Alternative oxidase inhibitors as antiparasitic agents against scuticociliatosis.

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Philasterides dicentrarchi causes a severe disease in turbot, and at present there are no drugs available to treat infected fish. We have previously demonstrated that, in addition to the classical respiratory pathway, P. dicentrarchi possesses an alternative mitochondrial respiratory pathway that is

Suppression of mitochondrial oxygen metabolism mediated by the transcription factor HIF-1 alleviates propofol-induced cell toxicity.

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A line of studies strongly suggest that the intravenous anesthetic, propofol, suppresses mitochondrial oxygen metabolism. It is also indicated that propofol induces the cell death in a reactive oxygen species (ROS)-dependent manner. Because hypoxia-inducible factor 1 (HIF-1) is a transcription

Regulated function of the prolyl-4-hydroxylase domain (PHD) oxygen sensor proteins.

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Cellular oxygen is sensed by prolyl-4-hydroxylase domain (PHD) proteins that hydroxylate hypoxia-inducible factor (HIF) alpha subunits. Under normoxic conditions, hydroxylated HIFalpha is bound by the von Hippel-Lindau (pVHL) tumor suppressor, leading to ubiquitinylation and proteasomal degradation.

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