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aristolochic acid/atrophy
Veza se sprema u međuspremnik
Stranica 1 iz 52 rezultatima
[Nephropathy caused by Chinese plants and aristolochic acids: from clinical observation to experimental model].
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In 1992, a new type of progressive renal fibrosis was reported in patients after the intake of weight-reducing pills containing a Chinese herb (Aristolochia fangchi) rich of nephrotoxic and carcinogenic aristolochic acids (AA). Up to now, Chinese herb nephropathy (CHN), also called aristolochic acid
Human bone morphogenetic protein-7 does not counteract aristolochic acid-induced renal toxicity.
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Aristolochic acids (AA) are nephrotoxic and profibrotic agents, leading to chronic kidney disease. As some controversial studies have reported a nephroprotective effect of exogenous recombinant human bone morphogenetic protein (rhBMP)-7 in several models of renal fibrosis, we investigated the
Assessment of nephrotoxicity of herbal medicine containing aristolochic acid in mice.
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Characterization of cytotoxic effects of aristolochic acids on the vascular endothelium.
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Aristolochic acid nephropathy (AAN) is characterized by interstitial fibrosis, proximal tubular atrophy, and hypoxia. A correlation between a reduced peritubular capillary density and the severity of fibrosis has been demonstrated. As calcium, redox and energetic homeostasis are crucial in
[Establishment of model of aristolochic acid-induced chronic renal interstitial fibrosis in rats].
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OBJECTIVE
To study chronic renal interstitial fibrosis induced by aristolochic acid (AA) in animal models.
METHODS
Female Wistar rats were divided into two groups: AA group (n = 42) peritoneally injected with AA (5 mg.kg-1.d-1) for 16 weeks and control group (n = 5) peritoneally injected with normal
Phospholipase A2 inhibitors protect against prion and Abeta mediated synapse degeneration.
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BACKGROUND
An early event in the neuropathology of prion and Alzheimer's diseases is the loss of synapses and a corresponding reduction in the level of synaptophysin, a pre-synaptic membrane protein essential for neurotransmission. The molecular mechanisms involved in synapse degeneration in these
[Aristolochic acid induces renal tubular injury and inhibits expression of bone morphogenetic protein-7 mRNA in renal tissue of rats].
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OBJECTIVE
To investigate the pathogenic mechanism of aristolochic acid nephropathy (AAN) by observing the renal tubular injury and the change of the expression of bone morphogenetic protein-7 (BMP-7) mRNA in renal tissue of rats induced by aristolochic acid (AA), an active constituent in Caulis
Renal chymase-dependent pathway for angiotensin II formation mediated acute kidney injury in a mouse model of aristolochic acid I-induced acute nephropathy.
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Angiotensin-converting enzyme (ACE) is the primary enzyme that converts angiotensin I (Ang I) to angiotensin II (Ang II) in the renin-angiotensin system (RAS). However, chymase hydrates Ang I to Ang II independently of ACE in some kidney diseases, and it may play an important role. The present study
[Traditional remedy-induced Chinese herbs nephropathy showing rapid deterioration of renal function].
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A 19-year-old female was referred to our hospital for azotemia and anemia. She had been taking a health food for atopic dermatitis for about three years. Urinalysis showed proteinuria, glycosuria and microscopic hematuria. Generalized aminoaciduria was observed. Moreover, severe anemia, azotemia,
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
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,
[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
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
Pharmacokinetics of p-Aminohippuric Acid and Inulin in Rabbits with Aristolochic Acid Nephropathy.
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The characteristics of aristolochic acid nephropathy (AAN) are interstitial fibrosis and atrophy of the proximal tubules, but with no change in glomeruli. To investigate the effects of AA on renal functions and the pharmacokinetics (PKs) of p-aminohippuric acid (PAH) and inulin, New Zealand white
Blockade of the mTOR signaling pathway with rapamycin ameliorates aristolochic acid nephropathy.
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Chronic aristolochic acid nephropathy (CAAN) is characterized by widespread apoptosis and interstitial fibrosis, which severely impairs kidney function. mTOR is crucial for cell proliferation and protein synthesis. In the present study, the therapeutic effects of blockade of mTOR activity by
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