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. 2022 May 16;37(3):432–443. doi: 10.3803/EnM.2021.1336

Fig. 5.

Fig. 5.

Short-chain fatty acids (SCFAs) affected autophagy and renal fibrosis in diabetic mice through the histone deacetylase (HDAC2)/unc51 like autophagy activating kinase 1 (ULK1) axis. (A) The ULK1 promoter region in the University of California Santa Cruz (UCSC) database had a peak for H3K27Ac. (B) ULK1 expression in the wild type (WT), diabetes (D)+sodium propionate (SP), D+sodium butyrate (SB), and D+sodium valproate (SV) mice renal medulla tissues and cells obtained from the renal cortex or medulla was measured by Western blots. (C) ULK1 promoter sequences bound to H3K27Ac in mice renal tissues and cells obtained from the renal cortex or medulla from the above five groups detected by chromatin immunoprecipitation (ChIP). (D) The kidneys from 14-week-old mice of four genotypes were weighed, with the ratio of kidney to body weight calculated. (E) The degree of renal medulla fibrosis in mice of four genotypes detected by Masson staining. (F) Light chain 3 (LC3) expression measured by immunochemistry (IHC) in mice of the four genotypes. (G) ULK1 expression in mice of the four genotypes detected by Western blots. One-way analysis of variance was used for comparisons among multiple groups, and the Tukey multiple-comparison test was used for post hoc multiple comparisons. The effect size between different experimental groups and control groups was >0.8. aP<0.05 compared with the WT group; bP<0.05 compared with the diabetes group; cP<0.05; dP<0.01; eP<0.01 (n=6).