The Nuclear factor kappa-light-chain-enhancer of activated B cells (NF-kB) represent family of structurally-related eukaryotic transcription factors which regulate diverse array of cellular processes including immunological responses, inflammation, apoptosis, growth & development. Increased expression of NF-kB has often been seen in many diverse diseases, suggesting the importance of genomic deregulation to disease pathophysiology. In the present study we focused on acute kidney injury (AKI), which remains one of the major risk factor showing a high rate of mortality and morbidity. The pathology associated with it, however, remains incompletely known though inflammation has been reported to be one of the major risk factor in the disease pathophysiology. The role of NF-kB thus seemed pertinent. In the present study we show that high dose of folic acid (FA) induced acute kidney injury (AKI) characterized by elevation in levels of blood urea nitrogen & serum creatinine together with extensive tubular necrosis, loss of brush border and marked reduction in mitochondria. One of the salient observations of this study was a coupled increase in the expression of renal, relA, NF-kB2, and p53 genes and proteins during folic acid induced AKI (FA AKI). Treatment of mice with NF-kB inhibitor, pyrrolidine dithio-carbamate ammonium (PDTC) lowered the expression of these transcription factors and ameliorated the aberrant renal function by decreasing serum creatinine levels. In conclusion, our results suggested that NF-kB plays a pivotal role in maintaining renal function that also involved regulating p53 levels during FA AKI.

Nuclear factor-κB (NF-κB) is a critical regulator of inflammation and stress response signaling in acute kidney injury (AKI). Increasing evidence demonstrates that NF-κB signaling is directly related to oxidative stress, autophagy, mitochondrial malfunction, and apoptosis in the process of AKI. Injury-related stimuli, including ischemia–reperfusion, sepsis, nephrotoxins, reactive oxygen species (ROS) and damage-associated molecular patterns (DAMPs), activate canonical and non-canonical NF-κB pathways, resulting in renal inflammation and tubular injury. Recent investigations have shown that TLR4/NF-κB signaling, NLRP3 inflammasome activation, defective autophagy, and mitochondrial dysfunction mediate inflammatory and pro-apoptotic responses in AKI. On the other hand, autophagy-associated proteins such as microtubule-associated protein 1 light chain 3 beta (LC3B) and Beclin-1 may play renoprotective roles through the regulation of NF-κB signaling. This review tries to cover the knowledge regarding NF-κB signaling in AKI and to emphasize the possible function of NF-κB signaling in the control of inflammation, autophagy, and apoptosis. It also seeks to provide some insight into future research directions that may guide the development of more effective therapies for AKI.