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1.
Nagoya J Med Sci ; 81(3): 439-452, 2019 Aug.
Artículo en Inglés | MEDLINE | ID: mdl-31579334

RESUMEN

Pseudomonas aeruginosa is capable of biofilm formation. In this study, we investigated the effects of aqueous Tradescantia pallida extract on Pseudomonas aeruginosa growth and biofilm formation. Aqueous Tradescantia pallida extracts significantly inhibited both bacterial growth and biofilm formation. However, methanolic Tradescantia pallida extracts inhibited neither. Aqueous Tradescantia pallida extracts were deactivated by heating but were not deactivated by light exposure. The ingredients retained the inhibitory effect on the bacterial growth and biofilm formation after ultrafiltration of aqueous Tradescantia pallida extract. Furthermore, polyphenol-rich Tradescantia pallida extracts inhibited bacterial growth, thus, polyphenols are possible to be an active ingredient. We observed the biofilm by scanning electron microscopy, and quantitative and qualitative differences in the biofilm and cells morphology. Interestingly, the biofilm treated aqueous Tradescantia pallida extracts remained premature. We postulated that premature biofilm formation was due to the inhibition of swarming motility. Indeed, aqueous Tradescantia pallida extracts inhibited swarming motility. These results demonstrate that Peudomonas aeruginosa growth and biofilm formation are inhibited by aqueous Tradescantia pallida extracts.


Asunto(s)
Antibacterianos/química , Antibacterianos/farmacología , Extractos Vegetales/química , Extractos Vegetales/farmacología , Pseudomonas aeruginosa/efectos de los fármacos , Tradescantia/química , Biopelículas/efectos de los fármacos
2.
Toxins (Basel) ; 6(9): 2594-604, 2014 Aug 25.
Artículo en Inglés | MEDLINE | ID: mdl-25157606

RESUMEN

A novel hemorrhagic metalloproteinase, okinalysin, was isolated from the venom of Ovophis okinavensis. It possessed caseinolytic and hemorrhagic activities, and also hydrolyzed fibrinogen and collagen. These activities were inhibited by ethylenediaminetetraacetic acid (EDTA) but not by p-amidinophenyl methanesulfonyl fluoride hydrochloride (APMSF). The molecular mass of okinalysin was 22,202 Da measured by MALDI/TOF mass spectrometry. The primary structure of okinalysin was partially determined by Edman sequencing, and the putative zinc-binding domain HEXXHXXGXXH was found to be present in its structure. From these data, okinalysin is defined as a metalloproteinase belonging to a P-I class. The partial amino acid sequence of okinalysin was homologous to the C-terminus of MP 10, a putative metalloproteinase induced from transcriptome of the venom gland cDNA sequencing of O. okinavensis. Okinalysin possessed cytotoxic activity on cultured endothelial cells, and the EC50 on human pulmonary artery endothelial cells was determined to be 0.6 µg/mL. The histopathological study also showed that okinalysin causes the leakage of red blood cells and neutrophil infiltration. These results indicate that destruction of blood vessels by okinalysin is one of the main causes of hemorrhage.


Asunto(s)
Venenos de Crotálidos/química , Células Endoteliales/efectos de los fármacos , Metaloproteasas/farmacología , Secuencia de Aminoácidos , Animales , Caseínas/metabolismo , Supervivencia Celular/efectos de los fármacos , Células Cultivadas , Colágeno Tipo IV/metabolismo , Venenos de Crotálidos/aislamiento & purificación , Venenos de Crotálidos/farmacología , Células Endoteliales/metabolismo , Fibrinógeno/metabolismo , Hemorragia/inducido químicamente , Humanos , Hidrólisis , Metaloproteasas/química , Metaloproteasas/aislamiento & purificación , Ratones , Datos de Secuencia Molecular , Fibras Musculares Esqueléticas/efectos de los fármacos , Fibras Musculares Esqueléticas/patología , Arteria Pulmonar , Muslo , Viperidae
3.
Eur J Pharmacol ; 552(1-3): 123-30, 2006 Dec 15.
Artículo en Inglés | MEDLINE | ID: mdl-17059816

RESUMEN

Each individual and pure catechin isolated from green tea was investigated as to its myocardial or blood pressure effects. The nitric oxide (NO) electrode and fluorometry were used to monitor changes in the NO and Ca(2+) contents of the heart, together with simultaneous recordings of the left ventricular developed pressure. The low dose of (-)-epigallocatechin-3-gallate (EGCg: 10(-6), 10(-5 )M) increased the left ventricular developed pressure with elevation of the transient fura-2 Ca(2+) signal (T(Ca)), but the high dose of EGCg (10(-4 )M) produced a maximum left ventricular developed pressure with decreases in the basal level of T(Ca) in a manner similar to the administration of the Ca-sensitizer pimobendan. However, the level of the transient NO signal (T(NO)) increased dose-dependently without any increases in the width of T(NO). In the isolated right atria, the contractile force of (-)-gallocatechin-3-gallate (GCg) at 10(-8)-10(-4 )M produced the highest pD(2) value, 6.7, in catechins (EGCg: 5.2, pimobendan: 5.1), but did not affect the heart rate. GCg, an artifact due to the epimerization of EGCg during the heating procedure, showed the most prolonged hypotensive effect in rabbits among the catechins. Each catechin (GCg or EGCg), like the NO donor, may have a therapeutic use as an NO-mediated vasorelaxant and may have an additional protective action in myocardial ischemia-reperfusion induced injury.


Asunto(s)
Cardiotónicos/farmacología , Catequina/farmacología , Corazón/efectos de los fármacos , Té/química , Animales , Presión Sanguínea/efectos de los fármacos , Calcio/metabolismo , Catequina/análogos & derivados , Catequina/aislamiento & purificación , Relación Dosis-Respuesta a Droga , Inhibidores Enzimáticos/farmacología , Femenino , Cobayas , Corazón/fisiología , Ventrículos Cardíacos/efectos de los fármacos , Técnicas In Vitro , Masculino , Miocardio/citología , Miocardio/metabolismo , NG-Nitroarginina Metil Éster/farmacología , Óxido Nítrico/metabolismo , Óxido Nítrico Sintasa/antagonistas & inhibidores , Perfusión , Piridazinas/farmacología , Conejos , Transducción de Señal/efectos de los fármacos , Vasodilatadores/farmacología , Función Ventricular , Presión Ventricular/efectos de los fármacos
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