Abstract: The Nuclear Factor- k B (Nf-k B) is a Factor of Transcription (FT) ubiquitin preserved in the eukaryotic cells. Nf-k B is activated by numerous stimuli including viral and bacterial products, ultraviolet radiations, oxidant radicals, cytokines and various chemical substances. Once activated, Nf-k B directly checks, or with the cooperation of other factors of transcription, the activity of over 100 genes that produce cytokines, factors of growth, chemokines, molecules of adhesion, proteins of the acute phase. The transcriptional factor NF-k B is implicated in the pathogenesis of chronic inflammatory disease of the vascular system and in the process of formation of atherosclerotic lesions. In fact, NF-k B, in the activated state, is identified in situ in atherosclerotic human plates, while itís absent in vases exempted by atherosclerotic lesions. Recent study has shown that the infection by HSV-1 is able to activate NF-k B in persistent way and to higher levels respect to the others deriving from subsequent exposure to inflammatory cytokines in various types of human cells. Moreover, the virus interferes with the self-regulating system of NF-k B, with consequent exacerbation of the inflammatory state. For this reason, NF-k B could represent an interesting target for new chemotherapic drugs with anti-viral action and anti-inflammatory in the herpetic infections. The biggest part of the anti-inflammatory actions of the Glucocorticoids (GC) depends by their ability to interfere with the functions of transcription factors, such as NF-k B. Tissue lesions, cytokines, free radicals and oxidized damages induce the activation of the NF-k B, whose action determines increase of the synthesis of COX2 and therefore of the production of some prostaglandins with pro-inflammatory function. Finally, the inhibition of the COX2 and NF-k B operated by the FANSs has shown, in some cases, benefits anticancer effects. For all of these influences on many pathologic processes, Nf-k B can be considered as target of pharmacological treatment and object of continuous studies.
G.A. Scardina , A. Ruggieri , F. Carini , A. Cacioppo , V. Valenza and P. Messina , 2007. Nf-k B as Target of Pharmacological Treatment. Research Journal of Biological Sciences, 2: 403-407.