NF-κB signaling pathway and free radical impact.

Abstract

The activation of NF-κB transcription factor is critical for a wide range of processes such as immunity, inflammation, cell development, growth and survival. It is activated by a variety of stimuli including cytokines, ionizing radiation and oxidative stress. Redox modulations of NF-κB pathway have been widely demonstrated. Studies carried out during last years have advanced our knowledge about possible connections between NF-κB pathway and the impact of free radicals. This review is an endeavor to gather recent results focused on this issue, although an important question, whether oxidative stress plays a physiological role in NF-κB activation, seems to be still unanswered.

All-trans retinoic acid prevents epidural fibrosis through NF-κB signaling pathway in post-laminectomy rats

“…The NF-kB transcription factor is down stream of the NF-kB signaling pathway that regulates genes involved in cell growth regulation, inflammation and other biological activities (Siomek, 2012). The signaling events that lead to NF-kB activation involve phosphorylation, ubiquitination, and proteolytic degradation of cytosolic IkB, followed by translocation of the active dimer (p65/p50) into the nucleus, where it binds to cognate DNA sequences to activate transcription of target genes (Barnes and Karin, 1997).…”

NEFAs activate the oxidative stress-mediated NF-κB signaling pathway to induce inflammatory response in calf hepatocytes

“…Clinical investigation has shown that dairy cows with ketosis exhibit oxidative stress during the transition period [12,18,20]. An imbalance in oxidants/antioxidants, an excess of oxidants and/or a depletion of antioxidants, can lead to oxidative stress, which mainly characterized by overproduction of ROS include superoxide anion (O 2 À ), hydroxyl radical (OH), and their molecular by-products (e.g., hydrogen peroxide H 2 O 2 ) in the body [15,41,42]. Overproduction of ROS has been closely related with oxidative stress, which is characterized with a major shift in the cellular redox balance and usually accompanied by ROS-mediated damage [42].…”

“…Normally, the transcription factor NF-kB is sequestered in the cytoplasm bound to its inhibitor IkBa, whose phosphorylation is dependent on IKKb activity. Once stimulated by some stimuli, NF-kB unit p65 separates from IkB and translocates into the nucleus where NF-kB can regulate the transcription of several inflammatory cytokines genes, for example tumor necrosis factor alpha (TNF-a), interleukin 6 (IL-6) and interleukin 1 beta (IL-1b) [13][14][15]. In vitro studies have demonstrated that hepatocytes express components of the NFkB pathway in human and rodents [16,17].…”

Melatonin Protects Methamphetamine-Induced Neuroinflammation Through NF-κB and Nrf2 Pathways in Glioma Cell Line

“…However, the molecular mechanism by which METH induces inflammation in astrocyte cells remains unclear. It is well known that inflammation is the tight modulation of nuclear factor-jB (NF-jB) signal by inducing the degradation of inhibitory jBa (IjBa) and the nuclear translocation of p65 subunit, causing the release of inflammatory cytokines or cytotoxic productions [22][23][24]. Therefore, the inhibition of NF-jB signaling may be beneficial in protecting from the inflammation response and death of cells.…”