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Fig. 2 | Molecular Medicine

Fig. 2

From: The interaction between autophagy and the epithelial-mesenchymal transition mediated by NICD/ULK1 is involved in the formation of diabetic cataracts

Fig. 2

Rapamycin activated autophagy and inhibited the EMT in LECs from diabetic rats. Diabetic rats (DC) were induced by STZ. Rats in the normal control group (NC) were injected with the corresponding volume of citric acid-sodium citrate buffer. Diabetic rats were treated with DMSO solvent (DMSO) and rapamycin (RAPA) for 8 weeks respectively. Levels of the LC3 and SQSTM1/p62 proteins in the LECs of rats in each group were detected using Western blotting at 8 w (A). Statistical analysis of the relative expression of LC3II/I B and SQSTM1/p62 (C), n = 3. D Representative TEM images of autophagosomes (arrows) in different groups, bar = 0.5 Âµm. E Quantification and statistical analysis of the number of autophagosomes, n = 5. F E-cadherin and α-SMA protein levels in LECs from rats in each group were detected using Western blotting at 8 w. Statistical analysis of the relative expression of E-cadherin G and α-SMA (H), n = 3. I Immunofluorescence staining for E-cadherin (red) and α-SMA (green) in LECs from the different groups, n = 3. Bar = 10 Âµm. ns indicates P > 0.05; *P < 0.05, **P < 0.01, ***P < 0.001 and ****P < 0.0001 vs. NC group; #P < 0.05, ##P < 0.01, ###P < 0.001 vs. DC group; ★P < 0.05, ★★P < 0.01 and ★★★P < 0.001 vs. DMSO group

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