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d mannitol/hypoxia
L'enllaç es desa al porta-retalls
5 resultats
Involvement of peroxynitrite and hydroxyradical generated from nitric oxide in hypoxia/reoxygenation injury in rat cerebrocortical slices.
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The changes in nitric oxide (NO) formation during hypoxia and reoxygenation were measured in slices of rat cerebral cortex, and the possible involvement of NO and its decomposition products, including peroxynitrite and hydroxyradical, in the hypoxia/reoxygenation injury was subsequently
Atrial natriuretic peptide attenuates high glucose-activated transforming growth factor-beta, Smad and collagen synthesis in renal proximal tubular cells.
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Atrial natriuretic peptide, besides its role in the regulation of volume homeostasis, has been noted to exert cytoprotective effects in several cell types from hypoxia. The present study was performed to explore the effect of ANP on high glucose-activated transforming growth factor-beta1
Cobalt chloride compromises transepithelial barrier properties of CaCo-2 BBe human gastrointestinal epithelial cell layers.
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BACKGROUND
Elevation of the transcription factor HIF-1 is a prominent mediator of not only processes that accompany hypoxia, but also the tumor microenvironment and tissue regeneration. This study uses mediators of "chemical hypoxia" to ask the question whether HIF-1α elevation in a healthy
Endothelin-1 mediated high glucose-induced epithelial-mesenchymal transition in renal tubular cells.
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OBJECTIVE
The pathogenesis of interstitial fibrosis in diabetic nephropathy (DN) is an intractable problem without good therapy. Emerging evidence suggests that epithelial-mesenchymal transition (EMT) is an important mechanism for tubular epithelial cells undergoing profibrotic change in DN.
Excitatory amino acid release and free radical formation may cooperate in the genesis of ischemia-induced neuronal damage.
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Excessive stimulation of excitatory amino acid (EAA) receptors and abnormal production of oxygen-derived free radicals have repeatedly been implicated in the series of events linking brain hypoxia or ischemia to neuronal death. We report here that in rat hippocampal slices the KCl-stimulated output
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