**2. NF-**κ**B: redox sensitive transcription factor**

NF-κB plays an important role in regulating the immune and inflammatory response. NF-κB is a ubiquitous transcription factor [16]. p52/p100, NF-κB p50/ p105, C-REL, RELA/p65 and RelB constitute the Nuclear factor-κB (NF-κB) family of transcription factors. These factors mediate the transcription of target genes by binding to a specific DNA element, κB enhancer, as various hetero- or homo-dimers [17]. They also regulate the various biological responses such as immune responses, cell differentiation, cell proliferation, survival, stress response and inflammation. But the most studied and well-known function of NF-κB is in the inflammation, regulating the pro inflammatory cytokines, activation, differentiation and effector functions of T cells [18]. NF-κB has the ability to detect the stimuli such as infectious agents, UV radiation, ROS, Tissue injury, lipopolysaccharide (LPS), and free radicals which activate NF-κB [19]. The basic mechanism involves the tissue injury which activates NF-κB, dissociates IκB as a result of which the NF-κB enters the cell nucleus and activate the DNA to enhance the inflammatory cytokines [20]. Regulation of NF-κB activity is achieved through various post-translational modifications of the core components of the NF-κB signaling pathways. There are two pathways by which NF-κB is regulated; the canonical and the alternative pathway [21]. The canonical pathway is responsible for the installation of pro inflammatory cytokines, chemokines and other inflammatory mediators which directly engage into inflammation and act indirectly. Activation of the non-canonical NF-κB pathway involves different signaling molecules and leads to the predominant activation of the p52/RelB dimer. An "alternative" NF-κB pathway is activated by TNF-family cytokines—lymphotoxin b (TNFSF3) CD40 ligand (CD40L and TNFSF5), B cell activating factor (BAFF and TNFSF13B), and receptor activator of NF-κB ligand (RANKL and TNFSF11).
