Fig. 1: Poor outcomes of IRI were attenuated in Ripk3 or/and Mlkl deficiency mice.
From: RIPK3-MLKL-mediated necroinflammation contributes to AKI progression to CKD
a–f The kidneys and blood samples in mice were harvested at the indicated time following IRI (n = 8). a Freshly isolated proximal tubules were collected for Western blot to analyze of RIPK1, RIPK3, MLKL and caspase 8. b Representative electron micrographs of alive and necrotic PTCs are shown. Bar = 2 μM. c, d Serum BUN and creatinine levels were detected. e Representative images of PAS-stained kidney sections are shown. Bar = 100 μM. f Histologic damage in the outer medulla after IRI were scored by Periodic acid–Schiff (PAS) staining at 2 and 14 days after IRI. The degree of renal injury was assessed morphologically in the outer medulla regions of PAS-stained kidney sections. For counting, ten randomly selected fields per kidney were used. The percentage of tubules that displayed tubular necrosis, cast formation, and tubular dilation was scored semiquantitatively. ##P < 0.01 vs. Sham IRI, **P < 0.01 vs. WT IRI
