NF-kappaB Signaling Pathways in Neurological Inflammation: A Mini Review

The NF-kappa B (nuclear factor K-light-chain-enhancer of activated B cells) transcription factor family is a pleiotropic regulator of many cellular signaling pathways, providing a mechanism for the cells in response to a wide variety of stimuli linking to inflammation. The stimulated cells will be regulated by not only the canonical but also non-canonical NF-kappa B pathways. To initiate both of these pathways. I kappa B-degradation triggers NF-kappa B release and the nuclear translocated-heterodimer (or homodimer) can associate with the kappa B sites of promoter to regulate the gene transcriptions. NF-kappa B ubiquitously expresses in neurons and the constitutive NF-kappa B activation is associated with processing of neuronal information. NF-kappa B can regulate the transcription of genes such as chemokines, cytokines, proinflammatory enzymes, adhesion molecules, proinflammatory transcription factors, and other factors to modulate the neuronal survival. In neuronal insult. NF-kappa B constitutively active in neuron cell bodies can protect neurons against different injuries and regulate the neuronal inflammatory reactions. Besides neurons, NF-kappa B transcription factors are abundant in glial cells and cerebral blood vessels and the diverse functions of NF-kappa B also regulate the inflammatory reaction around the neuronal environment. NF-kappa B transcription factors are abundant in the brain and exhibit diverse functions. Several central nerve system (CNS) diseases are linked to NF-kappa B activated by inflammatory mediators. The RelA and c-Rel expression produce opposite effects on neuronal survival. Importantly, c-Rel expression in CNS plays a critical role in anti-apoptosis and reduces the age-related behaviors. Moreover, the different subunits of NF-kappa B dimer formation can modulate the neuroninflammation, neuronal protection, or neurotoxicity. The diverse functions of NF-kappa B depend on the subunits of the NF-kappa B dimer-formation which enable us to develop a therapeutic approach to neuroinflammation based on a new concept of inflammation as a strategic tool in neuronal cells. However, the detail role of NF-kappa B in neuroinflammation, remains to be clarified. In the present article, we provide an updated review of the current state of our knowledge about relationship between NF-kappa B and neuroinflammation.