C/EBPβ–TFAM-Mediated NLRP3 Inflammasome Activation Contributes to Arsenic-Induced Rat Kidney Injury

Compelling evidence has demonstrated that arsenic (As) exposure is associated with kidney injuries. Given inflammatory responses and immune imbalances are the root causes of several diseases, this study investigated potential mechanisms underlying NLRP3 inflammasome activation in As-induced injury. A rat model sub-chronic As was established via oral administration NaAsO2. The results revealed urinary β-2-microglobulin (β2-MG), N-acetyl-β-D-glucosidase (NAG) albumin (ALB) were increased As-exposed group, reflecting impairment. Moreover, significant glomerular vacuole-like changes, tubular dilatation cell infiltration observed. Meanwhile, expression levels neutrophil gelatinase-associated lipocalin (NGAL), IL-1β IL-18 enhanced tissues As-treated rats. Further, NLRP3, ASC caspase-1, which inflammasome-associated proteins, observed rats groups. upstream regulators C/EBPβ TFAM also elevated. These findings suggest triggers tissue impairs function. may be related to C/EBPβ–TFAM pathway pathway.