aristolochic acid/turse

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Edema-inducing activity of phospholipase A2 purified from human synovial fluid and inhibition by aristolochic acid.

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A neutral-active, Ca2+-dependent phospholipase A2 (PLA2) purified 11,000-fold from human synovial fluid (HSF) induced edema when injected into the mouse foot pad. The edema produced by HSF-PLA2 was dose-dependent and was positively correlated with the dose-dependent in vitro expression of PLA2

Characterization of three edema-inducing phospholipase A2 enzymes from habu (Trimeresurus flavoviridis) venom and their interaction with the alkaloid aristolochic acid.

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A basic phospholipase A2 (PLA2) enzyme, TFV PL-X (pI 9.2) and two acidic PLA2 enzymes, TFV PL-Ia (pI 4.9) and TFV PL-Ib (pI 4.5) were purified from Trimeresurus flavoviridis venom on CM-Sephadex C-25 and QAE-Sephadex A-25 columns, respectively. The basic enzyme exists as a monomer, whereas the

Interaction of aristolochic acid with Vipera russelli phospholipase A2: its effect on enzymatic and pathological activities.

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Aristolochic acid, an alkaloid from the plant Aristolochia species, interacts with the major basic phospholipase A2 from Vipera russelli venom. It is an uncompetitive inhibitor with a Ki of 9.9 X 10(-4)M when phosphatidylcholine is used as substrate. The inhibition of direct and indirect hemolysis

An unusual cause of hypokalemic paralysis: aristolochic acid nephropathy with Fanconi syndrome.

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Aristolochic acid nephropathy (AAN) with Fanconi syndrome presenting as hypokalemic paralysis is extraordinarily rare and may be unrecognized. We describe a 41-year-old man who presented with the inability to ambulate upon awakening in the morning. Physical examination revealed symmetric paralysis

Pharmacologic modulation of D-49 phospholipase A2-induced paw edema in the mouse.

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Paw edema was produced in CD-1 mice by the injection of 0.3 micrograms of snake venom PLA2 (A.p. piscivorus D-49) into the hind paw. Edema peaked at 10 min, remained elevated until 60 min, and then declined slowly. The PLA2 inhibitors, luffariellolide and aristolochic acid, reduced the edema but

Preliminary studies on phospholipase A2-induced mouse paw edema as a model to evaluate antiinflammatory agents.

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Phospholipase A2 (PLA2) is a key component of the inflammatory process because of its role in the generation of eicosanoids and platelet-activating factor (PAF). Manipulation of PLA2 activity offers a novel therapeutic approach for the development of antiinflammatory agents; however, there is a need

Aristolochic acid-induced Fanconi's syndrome and nephropathy presenting as hypokalemic paralysis.

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Hypokalemic paralysis rarely is seen as the presenting feature in patients with Fanconi's syndrome. We describe a 60-year-old man who presented with the inability to ambulate on awakening in the morning. The pertinent history revealed he had consumed Chinese herbs for leg edema for 5 months.

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

Evaluation of nephrotoxic effects of aristolochic acid on zebrafish (Danio rerio) larvae.

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To analyze the toxic effects of aristolochic acid (AA) on developed kidneys in zebrafish larvae, zebrafish at 3 days postfertilization were treated with various concentrations of AA for 24 h before the status of kidney injury was investigated from several points of view. It was found that 21% of the

Effects of aristolochic acid on phospholipase A2 activity and arachidonate metabolism of human neutrophils.

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Aristolochic acid is an alkaloid which has recently been shown to have anti-inflammatory activity against edema in mouse foot pads induced by phospholipases A2 from human synovial fluid. The present study has investigated the effects of aristolochic acid on phospholipase activity and arachidonic

[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

Aristolochic acid and its derivatives as inhibitors of snake venom L-amino acid oxidase.

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Snake venom L-amino acid oxidase (LAAO) exerts toxicity by inducing hemorrhage, pneumorrhagia, pulmonary edema, cardiac edema, liver cell necrosis etc. Being well conserved, inhibitors of the enzyme may be synthesized using the template of the substrate, substrate binding site and features of the

Cellular and topical in vivo inflammatory murine models in the evaluation of inhibitors of phospholipase A2.

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Several novel inhibitors of human synovial fluid phospholipase A2 (HSF-PLA2) were evaluated in cellular models of inflammatory mediator release (murine macrophage and human neutrophil) and topical in vivo inflammatory skin models in mice to ascertain the scope of effects which might be observed for

Structure-function relationships among neurotoxic phospholipases: NN-XIII-PLA2 from Indian cobra (Naja naja naja) and VRV PL-V from Russell's viper (Vipera russelli) venoms.

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Though venom phospholipases induce various pharmacological effects their mechanism of action is in some cases unclear. There may be separate pharmacological sites on the venom phospholipase molecule. In order to understand the structure-function relationships among venom phospholipases, studies on

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