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aristolochic acid/nekrose
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Side 1 fra 52 resultater
[Differential changes of intrarenal oxygenation in rat models of acute tubular necrosis caused by aristolochic acid and gentamicin].
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OBJECTIVE
To investigate the characteristics of renal oxygenation status in aristolochic acids I (AA-I) induced ATN rat model by method of blood oxygenation level-dependent MRI (BOLD-MRI) and compare it with ATN model caused by gentamicin.
METHODS
28 male Wistar rats were randomly divided into
Probenecid prevents acute tubular necrosis in a mouse model of aristolochic acid nephropathy.
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Experimental aristolochic acid nephropathy is characterized by early tubulointerstitial injury followed by fibrosis, reproducing chronic lesions seen in humans. In vitro, probenecid inhibits aristolochic acid entry through organic anion transporters, reduces specific aristolochic acid-DNA adduct
Possible mechanisms explaining the tendency towards interstitial fibrosis in aristolochic acid-induced acute tubular necrosis.
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BACKGROUND
We explored possible mechanisms responsible for the inability of plerosis and the tendency towards fibrosis in aristolochic acid-induced acute tubular necrosis (AA-ATN).
METHODS
Renal biopsy tissues from eight AA-ATN cases were examined. Tubulointerstitial injury was semiquantitatively
Assessment of nephrotoxicity of herbal medicine containing aristolochic acid in mice.
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[Effect of fermented cordyceps powder and prednisone on the Notch2/Hes-1 signaling activation in the kidney tubules of rats with acute aristolochic acid nephropathy].
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OBJECTIVE
To investigate the effect of both fermented Cordyceps powder (CS) and prednisone on the Notch2/hes-1 signaling activation in the kidney tubules of rats with acute aristolochic acid nephropathy (AAAN).
METHODS
Totally 50 SD rats were randomly divided into 4 groups, i.e., the normal group,
Bardoxolone methyl (BARD) ameliorates aristolochic acid (AA)-induced acute kidney injury through Nrf2 pathway.
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Bardoxolone methyl (BARD) is an antioxidant modulator that acts through induction of the nuclear factor erythroid 2-related factor 2 (Nrf2) signaling pathway. This study aimed to investigate the role of BARD in protecting kidneys from aristolochic acid (AA)-induced acute kidney injury (AKI). Male
Renal toxicity of aristolochic acid in rats as an example of nephrotoxicity testing in routine toxicology.
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The nephrotoxic action of aristolochic acid (AA) was investigated in female Wistar rats given single doses of 10, 50 or 100 mg/kg by gastric tube. Renal lesions developed within 3 days, the effect being dose-dependent. Histologically, there was evidence of necrosis of the epithelium of the renal
Low-dose darbepoetin alpha attenuates progression of a mouse model of aristolochic acid nephropathy through early tubular protection.
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OBJECTIVE
Aristolochic acid (AA) nephropathy, first reported as Chinese herbs nephropathy, is a rapidly progressive tubulointerstitial nephropathy that results in severe anemia, interstitial fibrosis and end-stage renal disease. Tubulointerstitial injury was studied in a mouse model of AA
Glutamate dehydrogenase requirement for apoptosis induced by aristolochic acid in renal tubular epithelial cells.
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Ingestion of aristolochic acids (AA) contained in herbal remedies results in a renal disease and, frequently, urothelial malignancy. The genotoxicity of AA in renal cells, including mutagenic DNA adduct formation, is well-documented. However, the mechanisms of AA-induced tubular atrophy and renal
Blocking TGF-β Signaling Pathway Preserves Mitochondrial Proteostasis and Reduces Early Activation of PDGFRβ+ Pericytes in Aristolochic Acid Induced Acute Kidney Injury in Wistar Male Rats.
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BACKGROUND
The platelet-derived growth factor receptor β (PDGFRβ)+ perivascular cell activation becomes increasingly recognized as a main source of scar-associated kidney myofibroblasts and recently emerged as a new cellular therapeutic target.
OBJECTIVE
In this regard, we first confirmed the
Acute toxicity of aristolochic acid in rodents.
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The acute toxic effects of aristolochic acid (AA) were tested in rats and mice of both sexes. Oral or intravenous administration in high doses was followed by death from acute renal failure within 15 days. Histologically, the predominant features were severe necrosis affecting the renal tubules,
On the histopathogenesis of rat forestomach carcinoma caused by aristolochic acid.
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The histopathogenesis of rat forestomach carcinoma induced experimentally with aristolochic acid was investigated. The intragastric administration of 10 mg/kg/day caused extensive necrosis of the squamous epithelium, followed by regeneration and hyperplasia, papilloma formation and ultimately by
[The clinical and pathological manifestations of aristolochic acid nephropathy--the report of 58 cases].
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OBJECTIVE
To realize and classify the aristolochic acid nephropathy (AAN) according to its clinical and pathological manifestations.
METHODS
Fifty eight cases in our Division during October 1998 to August 2001 were reviewed, and their clinical, laboratory and pathological manifestations as well as
[Studies on the renal toxicity caused by aristolochic acids (AAs) and Chinese herbs containing AAs].
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The article summarized the general situation of the study on the renal toxicity caused by aristolochic acids (AAs) and Chinese herbs containing AAs. The renal lesion induced by AAs and Chinese herbs containing AAs locates mainly in renal tubules, and glomeruluses have no obvious histological change.
Transgene-derived hepatocyte growth factor attenuates reactive renal fibrosis in aristolochic acid nephrotoxicity.
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BACKGROUND
Hepatocyte growth factor (HGF) has been demonstrated to attenuate acute tubular necrosis and interstitial fibrosis in a variety of rodent models of kidney disease. We investigated how HGF could affect chronic toxic nephropathy/interstitial fibrosis caused by aristolochic acid
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