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Journal of Korean Medical Science ; : 193-200, 2002.
Artículo en Inglés | WPRIM | ID: wpr-197892

RESUMEN

The involvement of NF-kappaB binding activity is known to be important in the mechanism of acute liver injury and in the induction of cyclooxygenase (COX-2). This study was performed to evaluate NF-kappaB binding activity and the expression of COX-2 in chronic liver injury induced by carbon tetrachloride (betaCCI(4)). Liver tissues from Sprague - Dawley rats were collected at 1, 3, 5, and 7th week after intraperitoneal injection of 0.1 mL of betaCCI(4)/100 g body weight twice a week. Reactive oxy-gen species (ROS) were measured in the postmitochondrial fraction by dichlorofluorescein formation with a fluorescent probe. An electrophoretic mobility shift assay was performed for NF-kappaB binding activity. Western blot was performed to measure the level of COX-1, COX-2, p65, p50, and I B proteins. ROS and NF-kappaB activity increased during the CCl4-induced chronic liver injury. The expression of nuclear p65 protein and p50 protein increased compared with that of the control, while the cytoplasmic I B protein decreased as the inflammation persisted. The expression of COX-2 in betaCCI(4)-treated rat liver increased compared with that of the control. It could be suggested that ROS produced by betaCCI(4) treatment increased NF-kappaB binding activity and thereby COX-2 expression, and these might be implicated in the progress of chronic liver damage.


Asunto(s)
Animales , Ratas , Transporte Biológico , Tetracloruro de Carbono/administración & dosificación , Intoxicación por Tetracloruro de Carbono/metabolismo , Núcleo Celular/metabolismo , Ciclooxigenasa 1 , Ciclooxigenasa 2 , Citoplasma/metabolismo , Proteínas I-kappa B/biosíntesis , Isoenzimas/biosíntesis , Hígado/efectos de los fármacos , Proteínas de la Membrana , FN-kappa B/antagonistas & inhibidores , Subunidad p50 de NF-kappa B , Prostaglandina-Endoperóxido Sintasas/biosíntesis , Unión Proteica , Ratas Sprague-Dawley , Especies Reactivas de Oxígeno , Factor de Transcripción ReIA
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