Fig. 6: Inhibition of PKR protected renal tubule against injury in experimental mouse models.

a Schematic of experimental approach in IRI mouse model with or without C16 treatment. b Left: WB of renal tubular p-PKR levels in IRI mouse model with or without C16 treatment. Right: quantification of renal tubular p-PKR levels (3 mice/group). c Left: Scr in IRI mouse model with or without C16 treatment. Right: urinary KIM-1 levels in IRI mouse model with or without C16 treatment (5 mice/group). d Left: H&E staining of kidney tissue sections from IRI mouse model with or without C16 treatment. Right: quantification of kidney disease score (5 mice/group). e Left: TUNEL assay of kidney tissue sections from IRI mouse model with or without C16 treatment. Right: quantification of apoptosis in kidney tissues (5 mice/group). f Schematic of experimental approach in UUO mice with or without C16 treatment. g Left: WB of renal tubular p-PKR levels in in UUO mice with or without C16 treatment. Right: quantification of renal tubular p-PKR levels (3 mice/group). h Left: Scr in UUO mouse model with or without C16 treatment. Right: urinary KIM-1 levels in UUO mice with or without C16 treatment (5 mice/group). i Left: H&E staining of kidney tissue sections from UUO mice with or without C16 treatment. Right: quantification of kidney disease score (5 mice/group). j Left: TUNEL assay of kidney tissue sections from UUO mice with or without C16 treatment. Right: quantification of apoptosis in kidney tissues (5 mice/group). Scale bars, 50 μm. The above experiments were successfully repeated three times. One-way ANOVA with Tukey’s multiple comparisons test was performed in b–e, g–j and the results were presented as mean ± SEM. Images of mouse in a, f were created with BioRender.com. Source data are provided as a Source Data file.