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. 2022 Jan 4;20:3. doi: 10.1186/s12951-021-01122-w

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© The Author(s) 2021

Open AccessThis article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated in a credit line to the data.

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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

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