In an experiment on rats with lipopolysaccharide-induced AKI/sepsis-associated AKI, it was demonstrated that H2S prevented the development of inflammation and oxidative stress by reducing the expression of TNF-α, IL-1β, MDA, MPO, H2O2, and caspase-1, as well as through inhibition of the TLR4/NLRP3 signaling pathway (Figure 8) [165]. This evidence concerns the gene CASP1 and acute kidney injury.