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. Author manuscript; available in PMC: 2023 Aug 11.
Published in final edited form as: Transl Res. 2022 Oct 13;253:31–40. doi: 10.1016/j.trsl.2022.10.001

Fig 4.

Fig 4.

Knockout of kidney proximal tubule PFKFB3 ameliorates cisplatin induced AKI in mice. Pfkfb3-WT and Pfkfb3-KO littermate mice were intraperitoneally injected with 30 mg/kg cisplatin or saline. Mice were euthanized at day 3 after injection to collect kidney tissues and blood samples. (A) Immunoblots of PFKFB3 in kidney cortex with cyclophilin B as internal loading control. (B) Immunohistochemical staining of PFKFB3 in renal cortex. Scale bar = 200 μm. (C) Representative immunoblot of cleaved caspase-3 in kidney cortical lysates from Pfkfb3-WT and Pfkfb3-KO mice with or without cisplatin treatment. Cyclophilin B was detected as internal loading control. (D) Representative H&E staining of kidney tissues. Scale bar = 200 μm. (E) Densitometry of cleaved caspase-3. The signal was normalized to the internal loading control. (F) Blood urea nitrogen. (G) Representative images of TUNEL staining. Scale bar = 200 μm. (H) Serum creatinine. (I) Histology scores of tubular injury. (J) Quantification of TUNEL-positive cells in kidney tissues. Data are expressed as means ±SD; n =5 mice for each group. *, P < 0.05 vs wild-type control groups; #, P < 0.05 vs cisplatin-treated wild-type group.