Open AccessRedox Regulation of Nuclear Factor Kappa B: Therapeutic Potential for Attenuating Inflammatory Responses
Author(s) -
Christman John W.,
Blackwell Timothy S.,
Juurlink Bernhard H.J.
Publication year - 2000
Publication title -
brain pathology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.986
H-Index - 132
eISSN - 1750-3639
pISSN - 1015-6305
DOI - 10.1111/j.1750-3639.2000.tb00252.x
Subject(s) - transcription factor , reactive oxygen species , oxidative stress , nfkb1 , lipid peroxidation , nf κb , endogeny , microbiology and biotechnology , chemistry , enzyme , keap1 , signal transduction , inflammation , biochemistry , biology , immunology , gene
Nuclear factor kappa B (NF‐κB) is a protein transcription factor that is required for maximal transcription of a wide array of pro‐inflammatory mediators that are involved in the pathogenesis of stroke. The purpose of this review article is to describe what is known about the molecular biology of NF NF‐κB and to review current understanding of the interaction between reactive oxygen species (ROS) in NF‐κB. ROS seem to play a duel role by participating in the NF‐κB activation cascade and by directly modulating DNA binding affinity. Exogenous and endogenous antioxidants are effective in blocking activation of NF‐κB and preventing the consequences of pro‐inflammatory gene expression. Phase II enzymes either directly or indirectly play a major in vivo role in minimizing oxidative stress by scavenging peroxides, peroxide breakdown products and dicarbonyls and in regeneration of lipid peroxidation chain‐breaker, vitamin E. Dietary phase II enzyme inducers have been demonstrated to increase phase II enzyme activities in a variety of tissues. These data, together, suggest that phase II enzyme inducers could have therapeutic value for ameliorating inflammatory conditions.