RESUMO
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.
Assuntos
Animais , Ratos , Transporte Biológico , Tetracloreto de Carbono/administração & dosagem , Intoxicação por Tetracloreto de Carbono/metabolismo , Núcleo Celular/metabolismo , Ciclo-Oxigenase 1 , Ciclo-Oxigenase 2 , Citoplasma/metabolismo , Proteínas I-kappa B/biossíntese , Isoenzimas/biossíntese , Fígado/efeitos dos fármacos , Proteínas de Membrana , NF-kappa B/antagonistas & inibidores , Subunidade p50 de NF-kappa B , Prostaglandina-Endoperóxido Sintases/biossíntese , Ligação Proteica , Ratos Sprague-Dawley , Espécies Reativas de Oxigênio , Fator de Transcrição RelARESUMO
A herbal hepatoprotective formulation Liv 52 down regulated the tumour necrosis factor (TNF) production in Charles Foster Rats treated with CCl4. Inhibition of TNF activity was proportional to the hepatoprotective activity.
Assuntos
Animais , Intoxicação por Tetracloreto de Carbono/metabolismo , Regulação para Baixo/efeitos dos fármacos , Combinação de Medicamentos , Doença Hepática Induzida por Substâncias e Drogas/metabolismo , Extratos Vegetais/farmacologia , Plantas Medicinais , Ratos , Fator de Necrose Tumoral alfa/biossínteseRESUMO
Effect of oral feeding of Liv-52, on lipid peroxidation in normal liver and damaged liver induced by CCl4 of albino rats was studied. While Liv-52 did not show any effect on normal healthy liver cells, it had a significant protective effect against damage by CCl4 as shown by significant decrease in malonaldialdehyde content.
Assuntos
Animais , Intoxicação por Tetracloreto de Carbono/metabolismo , Combinação de Medicamentos , Feminino , Doença Hepática Induzida por Substâncias e Drogas/metabolismo , Peroxidação de Lipídeos/efeitos dos fármacos , Masculino , Extratos Vegetais/farmacologia , Plantas Medicinais , RatosRESUMO
Effects of CCL4 on bile formation and on the hepatic bilirubin metabolism were studied in rats by recording the intrabiliary pressure and flow rate, BSP and bilirubin clearances and by estimating the activity of the hepatic enzyme, Uridine diphosphate (UDP) glucuronyl transferase. From the results of these studies it was concluded that: (i) CCl4 reduced the rate of bile secretion by the lever cells of the rats, (ii) spontaneous bile flow and choleretic response to dehydrocholate declined in the CCl4 treated rats, (iii) CCl4 reduced the clearance of BSP and bilirubin (UCB or BG) at low plasma concentrations as well as the absolute rate of BSP and bilirubin (UCB or BG) excretion when plasma levels were above those required to saturate active transport of the dye or hepatic excretory mechanisms of bilirubin, (iv) CCl4 produced a specific bilirubin conjugatory defect by inhibiting the activity of hepatic UDP-glucuronyl transferase and that (v) all these hepatotoxic effects of CCl4 appeared as early as 2-3 hours after its administration.