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Oxidative Medicine and Cellular Longevity
Volume 2013, Article ID 308358, 8 pages
Research Article

Influence of Block of NF-Kappa B Signaling Pathway on Oxidative Stress in the Liver Homogenates

1Experimental and Clinical Physiology, Department of Cardiovascular Physiology, Medical University of Lodz, 6/8 Mazowiecka Street, 92-215 Lodz, Poland
2Department of Biochemical Pharmacy, Department of Pharmacy, Medical University of Lodz, 1 Muszynskiego Street, 91-151 Lodz, Poland
3Laboratory of Molecular Diagnostic and Pharmacogenomics, Department of Biochemical Pharmacy, Medical University of Lodz, 1 Muszynskiego Street, 91-151 Lodz, Poland

Received 27 October 2012; Revised 18 February 2013; Accepted 19 February 2013

Academic Editor: Ron Kohen

Copyright © 2013 Paulina Kleniewska et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


The aim of the present study was to assess whether BAY 11-7082, a nuclear factor-kappaB (NF-κB) inhibitor, influences the level of reactive oxygen species (ROS), tumor necrosis factor alpha (TNF-α), and NF-κB related signaling pathways in the liver. The animals were divided into 4 groups: I: saline; II: saline + endothelin-1 (ET-1) (1.25 μg/kg b.w., i.v.); III: saline + ET-1 (12.5 μg/kg b.w., i.v.); and IV: BAY 11-7082 (10 mg/kg b.w., i.v.) + ET-1 (12.5 μg/kg b.w., i.v.). Injection of ET-1 alone at a dose of 12.5 μg/kg b.w. showed a significant ( ) increase in thiobarbituric acid reactive substances (TBARS) and hydrogen peroxide (H2O2) level and decrease ( ) in GSH level (vs. control). ET-1 administration slightly downregulated gene expression of p65 of NF-κB but potently and in a dose-dependent way downregulated p21-cip gene expression in the liver. BAY 11-7082 significantly decreased TBARS ( ), H2O2 ( ) and improved the redox status ( ), compared to ET-1 group. The concentration of TNF-α was increased in the presence of ET-1 ( ), while BAY 11-7082 decreased TNF-α concentration ( ). Inhibition of IkBα before ET-1 administration downregulated gene expression of p21-cip but had no effect on p65.