Therefore, the present study was conducted to answer the upcoming questions: (1) Does TLR4 crosstalk with NLPR3/IL-1β signaling in Cp-induced AKI, and if so; (2) Does the inhibition of TLR4 and NLRP3/IL-1β signaling play a role in NAC- and CGA-mediated nephroprotection against Cp-induced nephrotoxicity, and how is this nephroprotection effect associated with caspase 1/GSDMD-induced pyroptosis? Here, CASP1 is linked to acute kidney injury.