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protoporphyrin/hypoxia
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Sivu 1 alkaen 124 tuloksia
Tin protoporphyrin provides protection following cerebral hypoxia-ischemia: involvement of alternative pathways.
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The contribution of heme oxygenase (HO)-linked pathways to neurodegeneration following cerebral hypoxia-ischemia (HI) remains unclear. We investigated whether HO modulators affected HI-induced brain damage and explored potential mechanisms involved. HI was induced in 26-day-old male Wistar rats by
Hypoxia significantly reduces aminolaevulinic acid-induced protoporphyrin IX synthesis in EMT6 cells.
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We have studied the effects of hypoxia on aminolaevulinic acid (ALA)-induced protoporphyrin IX (PpIX) synthesis in EMT6 monolayer cultures characterized by different cell densities and proliferation rates. Specifically, after ALA incubation under hypoxic or normoxic conditions, we detected
Cobalt protoporphyrin pretreatment protects human embryonic stem cell-derived cardiomyocytes from hypoxia/reoxygenation injury in vitro and increases graft size and vascularization in vivo.
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Human embryonic stem cell-derived cardiomyocytes (hESC-CMs) can regenerate infarcted myocardium. However, when implanted into acutely infarcted hearts, few cells survive the first week postimplant. To improve early graft survival, hESC-CMs were pretreated with cobalt protoporphyrin (CoPP), a
Oxygen Availability for Porphyrin Biosynthesis Enzymes Determines the Production of Protoporphyrin IX (PpIX) during Hypoxia.
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5-Aminolevulinic acid (ALA), a precursor of porphyrin, is specifically converted to the fluorescent substance protoporphyrin IX (PpIX) in tumors to be used as a prodrug for photodynamic therapy and diagnosis. Hypoxia, a common feature of solid tumors, decreases the efficacy of ALA-based photodynamic
Blocking heme oxygenase-1 by zinc protoporphyrin reduces tumor hypoxia-mediated VEGF release and inhibits tumor angiogenesis as a potential therapeutic agent against colorectal cancer.
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BACKGROUND
Hypoxia in tumor niche is one of important factors to start regeneration of blood vessels, leading to increase survival, proliferation, and invasion in cancer cells. Under hypoxia microenvironment, furthermore, steadily increased hypoxia-inducible factor -1α (HIF-1α) is observed, and can
Erythrocyte zinc protoporphyrin is elevated with prematurity and fetal hypoxemia.
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OBJECTIVE
To examine the utility of red blood cell (RBC) zinc protoporphyrin/heme ratio (ZnPP/H) as an indicator of fetal iron status, because unfavorable neurodevelopmental outcomes have been associated with poor iron status at birth, as indicated by low serum ferritin, and because few reliable
Imaging of hypoxia, oxygen consumption and recovery in vivo during ALA-photodynamic therapy using delayed fluorescence of Protoporphyrin IX.
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BACKGROUND
Hypoxic lesions often respond poorly to cancer therapies. Particularly, photodynamic therapy (PDT) consumes oxygen in treated tissues, which in turn lowers its efficacy. Tools for online monitoring of intracellular pO2 areEffect of oxygen deficiency on cytochrome c, heme a, and iron protoporphyrin of L-cells.
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Signal transduction involved in lipoxin A4‑induced protection of tubular epithelial cells against hypoxia/reoxygenation injury.
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Previous studies have reported that lipoxin A4 (LXA4) may exert a renoprotective effect on ischemia/reperfusion injury in various animal models. The underlying mechanism of LXA4‑induced renoprotection during ischemia/reperfusion injury remains to be elucidated. The present study investigated
Cardioprotective and vasomotor effects of HO activity during acute and chronic hypoxia.
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Prolonged hypoxia leads to the development of pulmonary hypertension. Recent reports have suggested enhancement of heme oxygenase (HO), the major source of intracellular carbon monoxide (CO), prevents hypoxia-induced pulmonary hypertension and vascular remodeling in rats. Therefore, we hypothesized
Tanshinone IIA modulates pulmonary vascular response to agonist and hypoxia primarily via inhibiting Ca2+ influx and release in normal and hypoxic pulmonary hypertension rats.
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The present study was designed to investigate the vascular effects and underlying mechanisms of tanshinone IIA on isolated rat pulmonary artery. Isometric tension was recorded in the arteries from normal and hypoxic pulmonary hypertension rats under normoxia or hypoxia condition. The results showed
Correlation of HO-1 expression with onset and reversal of hypoxia-induced vasoconstrictor hyporeactivity.
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Rats exposed to chronic hypoxia (CH; 4 wk at 0.5 atm) exhibit attenuated renal vasoconstrictor reactivity to phenylephrine (PE). Preliminary studies from our laboratory suggest that this response is mediated by hypoxic induction of heme oxygenase (HO) and subsequent release of the endogenous
Interaction between endothelial heme oxygenase-2 and endothelin-1 in altered aortic reactivity after hypoxia in rats.
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The aim of this study was to determine whether increased expression of heme oxygenase (HO) contributes to impairment of aortic contractile responses after hypoxia through effects on reactivity to endothelin-1 (ET-1). Thoracic aortas from normoxic rats and rats exposed to hypoxia (10% O2) for 16 or
[Effects of hypoxia on heme oxygenase/carbon monoxide and type I collagen in pulmonary artery smooth muscle cells of rats].
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OBJECTIVE
To explore changes of expression of heme oxygenase (HO) and production of endogenous carbon monoxide in hypoxic pulmonary artery smooth muscle cells (PASMCs) of rats and study their effects on type I collagen under hypoxia.
METHODS
PASMCs of rats were cultured in vitro and incubated under
Role of vascular heme oxygenase in reduced myogenic reactivity following chronic hypoxia.
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OBJECTIVE
Exposure to chronic hypoxia (CH) results in a persistent endothelium-dependent vascular smooth muscle hyperpolarization that diminishes vasoconstrictor reactivity. Experiments were performed to test the hypothesis that products of both cytochrome P450 epoxygenase (CYP) and heme oxygenase
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