aristolochic acid/necrosis

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

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

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

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) 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

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

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

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

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

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,

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

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

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.

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