Fig. 5

CeNP-PEG inhibited aerobic glycolysis in UUO mice. A The schematic graph of the experimental design. B The expression of α-SMA, COL1, FN, HK2, PFKP and PKM2 was evaluated by RT-PCR analysis. β-actin was used as the control (^#P < 0.05 and ^##P < 0.01 for UUO vs. control, and ^*P < 0.05 and ^**P < 0.01 for UUO vs. UUO + CeNP-PEG or UUO + 2-DG; n = 3 for each group). (C, D and E) The expression of α-SMA, E-cadherin, Vimentin, FN, HK1, HK2, PFKP, and phosphorylated and total Smad2 and Smad3 was evaluated by western blot analysis. β-actin was used as the control. (^#P < 0.05 and ^##P < 0.01 for UUO vs. control, and ^*P < 0.05 and ^**P < 0.01 for UUO vs. UUO + CeNP-PEG or UUO + 2-DG; n = 3 for each group). F The lactate acid production was measured (^#P < 0.05 and ^##P < 0.01 for UUO vs. control, and ^*P < 0.05 and ^**P < 0.01 for UUO vs. UUO + CeNP-PEG or UUO + 2-DG; n = 3 for each group). G The mitochondrial membrane potential of cells isolated from UUO kidney in the absence or presence of CeNP-PEG or 2-DG was measured by flow cytometry. H The tubular injury scores of UUO mice after different treatments (^#P < 0.05 and ^##P < 0.01 for UUO vs. control, and ^*P < 0.05 and ^**P < 0.01 for UUO versus UUO + CeNP-PEG or UUO + 2-DG; n = 3 for each group). I The renal injury was evaluated by H&E staining. The renal fibrosis was evaluated by Masson trichrome and PAS staining, and immunohistochemical analysis was performed to determine the expression of α-SMA, E-cadherin and HK2