NF-kappaB Binding Activity and Cyclooxygenase-2 Expression in Persistent betaCCI(4)-Treated Rat Liver Injury.
10.3346/jkms.2002.17.2.193
- Author:
Sang Hyun KIM
1
;
Hyung Jun CHU
;
Dae Hwan KANG
;
Geun Am SONG
;
Mong CHO
;
Ung Suk YANG
;
Hyon Jeen KIM
;
Hae Young CHUNG
Author Information
1. Department of Medicine, Pusan National University College of Medicine, Busan, Korea.
- Publication Type:Original Article
- Keywords:
NF-kappaB;
Prostaglandin-Endoperoxide Synthase;
Carbon Tetrachloride;
Liver Failure, Chronic
- MeSH:
Animals;
Biological Transport;
Carbon Tetrachloride/administration & dosage/*adverse effects;
Carbon Tetrachloride Poisoning/*metabolism/pathology;
Cell Nucleus/metabolism;
Cyclooxygenase 1;
Cyclooxygenase 2;
Cytoplasm/metabolism;
I-kappa B Proteins/biosynthesis;
Isoenzymes/*biosynthesis;
Liver/drug effects/*injuries/pathology;
Membrane Proteins;
NF-kappa B/antagonists & inhibitors/*metabolism;
NF-kappa B p50 Subunit;
Prostaglandin-Endoperoxide Synthases/*biosynthesis;
Protein Binding;
Rats;
Rats, Sprague-Dawley;
Reactive Oxygen Species;
Transcription Factor RelA
- From:Journal of Korean Medical Science
2002;17(2):193-200
- CountryRepublic of Korea
- Language:English
-
Abstract:
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.
