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Ameliorative effect of hepatocyte growth factor on glycerol-induced acute renal failure with acute tubular necrosis.
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OBJECTIVE
Hepatocyte growth factor (HGF), a multi-potent growth factor, is known to promote regeneration of damaged renal epithelial cells. Glycerol injection into rats induces severe acute renal failure (ARF) with ischemia and tubular necrosis, a model which shares many features with human ARF or
Skin necrosis induced by extravasation of glycerol-containing peripheral parenteral nutrition formulation.
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Administration of parenteral nutrition (PN) via a peripheral vein has gained support over the last decade due to serious complications associated with central venous catheterization. Extravasation and tissue necrosis have been reported with both peripheral and central dextrose-containing PN
Angiotensin II and endothelin in the renal cortex during the evolution of glycerol-induced acute tubular necrosis.
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Hypertonic glycerol injection is one of the most frequently used models of experimental acute renal failure. Late structural changes such as interstitial fibrosis in the renal cortex and tubular atrophy have been detected after severe acute tubular necrosis (ATN). The aim of this study was to
Glycerol induced ARF in rats is mediated by tumor necrosis factor-alpha.
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Glycerol-induced acute renal failure (ARF) in rats is a model of acute trauma in which intra-muscular injection of 50% glycerol causes rapid myoglobinuria, oliguria, and a rapid reduction in glomerular filtration rate. We found that plasma tumor necrosis factor-alpha (TNF-alpha) is rapidly induced
The morphology of "acute tubular necrosis" in man: analysis of 57 renal biopsies and a comparison with the glycerol model.
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Renal biopsies from 24 patients with oliguric "acute tubular necrosis" (ATN) and 26 patients with non-oliguric ATN were compared with biopsies from 7 patients who had recently recovered from ATN and 20 control patients. Many morphologic changes were present in the biopsies of patients with ATN and
Long-term evolution of the acute tubular necrosis (ATN) induced by glycerol: role of myofibroblasts and macrophages.
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Late structural changes such as interstitial fibrosis in the renal cortex and tubular atrophy have been detected after severe acute tubular necrosis (ATN). The aim of this study was to investigate the expression of fibronectin, alpha-smooth muscle actin and macrophages during the evolution of the
Reduced Na-K-ATPase in distal nephron in glycerol-induced acute tubular necrosis.
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To further characterize changes in tubular Na-K-ATPase in acute tubular necrosis (ATN), segmental analysis was performed in rat nephrons. Na-K-ATPase was assayed in the following segments: proximal convolution (PC), proximal straight (PS), outer medullary thick ascending limb (MTAL), cortical thick
The effect of dietary sodium chloride and gamma-glutamyl dopa on tubular necrosis following glycerol administration in the rat.
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Renal ammoniagenesis in kidney slices from rats undergoing glycerol-induced acute tubular necrosis.
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THE PATHOGENESIS OF GLYCEROL-INDUCED RENAL TUBULAR NECROSIS.
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Subcutaneous fat necrosis, haemolysis without siderosis, and renal tubular atrophy following repeated glycerol injections.
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The effect of oxygen under pressure on glycerol-induced tubular necrosis in the rat.
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Caffeic acid phenethyl ester suppresses the production of adipocytokines, leptin, tumor necrosis factor -alpha and resistin, during differentiation to adipocytes in 3T3-L1 cells.
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We previously reported that caffeic acid phenethyl ester (CAPE) suppresses 3T3-L1 differentiation to adipocytes through the inhibition of peroxisome proliferator-activated receptor (PPAR) gamma, CCAAT/enhancer-binding protein (C/EBP) alpha, fatty acid synthase (Fas) and adipocytes-specific fatty
P16INK4a played a critical role in exacerbating acute tubular necrosis in acute kidney injury.
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Acute kidney injury (AKI) is a common clinical syndrome with high morbidity and mortality, which is mostly caused by acute tubular necrosis (ATN). AKI is associated with many factors, including cell senescence, inflammatory infiltration, apoptosis and excessive accumulation of reactive oxygen
Tumour necrosis factor (TNF)alpha as a regulator of fat tissue mass in the Mediterranean gilthead sea bream (Sparus aurata L.).
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The study was undertaken to analyze the lipolytic effect and transcriptional regulation of tumour necrosis factor (TNF)alpha in gilthead sea bream (Sparus aurata L.). The study was also focused on the transcriptional regulation and analysis of the 5-flanking region of lipoprotein lipase (LPL) in an
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