Redox regulation of nuclear factor kappa B: therapeutic potential for attenuating inflammatory responses

Nuclear factor kappa B (NF-kappaB) 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-kappaB and to review current understanding of the interaction between reactive oxygen species (ROS) in NF-kappaB. ROS seem to play a duel role by participating in the NF-kappaB activation cascade and by directly modulating DNA binding affinity. Exogenous and endogenous antioxidants are effective in blocking activation of NF-kappaB 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.