aristolochic acid/hypoxia

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[Influence of hypoxia caused by impairment of peritubular capillary on the progression of chronic aristolochic acid nephropathy].

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OBJECTIVE To investigate the manifestation of impairment of peritubular capillary (PTC) in chronic aristolochic acid nephropathy (CAAN) and the influence of hypoxia caused by PTC impairment on the progression of CAAN. METHODS Fifty-four Wistar rats were randomly divided into 2 groups: Group A (n =

Role of peritubular capillary loss and hypoxia in progressive tubulointerstitial fibrosis in a rat model of aristolochic acid nephropathy.

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OBJECTIVE To investigate the effects of peritubular capillary (PTC) loss and hypoxia on the progression of tubulointerstitial fibrosis in a rat model of aristolochic acid nephropathy (AAN). METHODS Female Wistar rats received Caulis aristolochiae manshuriensis (CAM) decoction by gavage for 8 weeks,

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

Ischemic injury underlies the pathogenesis of aristolochic acid-induced acute kidney injury.

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Aristolochic acid nephropathy (AAN) is a progressive tubulointerstitial renal disease caused by aristolochic acid intake. To determine the contribution of renal ischemia to the pathogenesis of AAN, we characterized changes in the expression of angiogenic factors and vasoactive substances, and then

[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

Protective effect of prostaglandin E1 on renal microvascular injury in rats of acute aristolochic acid nephropathy.

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BACKGROUND To investigate the renal microvascular injury in acute aristolochic acid nephropathy (AAN) and the protective effects of prostaglandin E1 (PGE1) in acute AAN. METHODS Female Sprague-Dawley rats were randomly divided into three groups. The rats in PGE1 group received Caulis Aristolochia

Aristolochic acid I and ochratoxin A differentially regulate VEGF expression in porcine kidney epithelial cells--the involvement of SP-1 and HIFs transcription factors.

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Aristolochic acid I (AAI) and ochratoxin A (OTA) cause chronic kidney diseases. Recently, the contribution of hypoxic injuries and angiogenic disturbances to nephropathies has been suggested, but underlying mechanisms have not been fully clarified yet. In porcine kidney epithelial cell line, LLC-PK1

Aristolochic acid induces renal fibrosis by arresting proximal tubular cells in G2/M phase mediated by HIF-1α

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Renal tubulointerstitial fibrosis (TIF) is a common pathological feature of aristolochic acid (AA) nephropathy (AAN). G2/M arrest of proximal tubular cells (PTCs) is implicated in renal fibrosis of AAN, but the upstream regulatory molecule remains unknown. Hypoxia inducible factor-1α (HIF-1α)

[Chemical constituents from rhizome of Menispermum dauricum and their anti-hypoxic activities].

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To study the chemical constituents from the rhizome of Menispermum dauricum,fifteen compounds,N-methylcorydaldine( 1),thalifoline( 2),stepholidine( 3),acutumine( 4),daurisoline( 5),acutumidine( 6),dauricicoline( 7),bianfugecine( 8),6-O-demethylmenisporphine( 9),bianfugedine( 10),dauricoside(

[Study on homologous bone marrow mesenchymal stem cells in repairing peri-tubular capillary cluster].

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OBJECTIVE To investigate the potential effect of homologous bone marrow mesenchymal stem cells (MSCs) on repairing peri-tubular capillary cluster (PTCC), and on improving renal tubular and mesenchymal hypoxia condition. METHODS Monocyte was purified from bone marrow, amplified and identified as MSCs

An immunofluorescence assay for extracellular matrix components highlights the role of epithelial cells in producing a stable, fibrillar extracellular matrix.

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Activated fibroblasts are considered major drivers of fibrotic disease progression through the production of excessive extracellular matrix (ECM) in response to signals from damaged epithelial and inflammatory cells. Nevertheless, epithelial cells are capable of expressing components of the ECM,

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