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Fig. 5 | Cardiovascular Diabetology

Fig. 5

From: Glycemic control by the SGLT2 inhibitor empagliflozin decreases aortic stiffness, renal resistivity index and kidney injury

Fig. 5

Empagliflozin rescues RECK deficiency in the diabetic kidney and in high glucose (HG)-treated renal proximal tubule cells. a Western blot analysis shows changes in RECK expression in kidneys from control (CkC), diabetic (DbC) and EMPA-treated diabetic (DbE) mice. The accompanying bar graph shows quantitative analysis of RECK protein expression as fold change from baseline in the CkC group. *p < 0.05 vs. CkC; p < 0.05 vs. DbC. b Immunofluorescence staining indicates high level of expression in proximal tubule cells and lesser expression in the glomerulus. Magnification = 63× and scale bars = 50 μm. c, d The SGLT2 inhibitor EMPA restores high glucose (HG)-induced inhibition in RECK expression in cultured human renal proximal tubule epithelial cells (HK-2). High glucose suppresses RECK expression in HK2 cells with mannitol serving as an osmotic control (c). EMPA pretreatment reversed HG-induced suppression in RECK expression (d). While representative immunoblots from three independent experiments are shown to the left, the intensities of immuno-reactive bands from all three experiments are summarized on the right. The values are mean ± SE. *p < 0.05 vs. low glucose, p < 0.05 vs. high glucose. *p < 0.05 vs. CkC; p < 0.05 vs. DbC

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