Wu et al. found that 18α-GL, the biologically active metabolite of GL, prevented FFA-induced lipid accumulation and cell apoptosis in in vitro HepG2 NAFLD models and also prevented high-fat-diet-induced hepatic lipotoxicity and liver injury in vivo rat NAFLD models. GA stabilized lysosomal membranes, inhibited cathepsin B expression and enzyme activity, inhibited mitochondrial cytochrome c release, and reduced FFA-induced oxidative stress [109] .