Whilenot affecting the cell viability (Figure 4A), diosgenin showed an antioxidative effectby attenuating the ROS generation (Figure 4B) and exerted an anti-inflammatory effectvia reducing the expression of inflammatory proteins, including IL-1β,IL-6, and TNF-α in the hypoxia-stimulated renal tubular epithelialcells (Figure 4C).Additionally, diosgenin reversed the expression of fibrotic and EMT-relatedproteins, including TGF-β, phospho-Smad2/3, collagen 1, E-cadherin,α-SMA, and vimentin, which are highly associated with AKI-to-CKDprogression (Figure 4D,E). This evidence concerns the gene TGFB1 and acute kidney injury.