Fig. 1: RDN effectively promoted urinary glucose excretion in DCM rats. | Laboratory Investigation

Fig. 1: RDN effectively promoted urinary glucose excretion in DCM rats.

From: Renal denervation ameliorates cardiac metabolic remodeling in diabetic cardiomyopathy rats by suppressing renal SGLT2 expression

Fig. 1

A RDN removed renal sympathetic nerves and attenuated sympathetic outflow. a Representative images of TH immunohistochemical staining in the renal vessels (magnification, 100×) and renal cortex (magnification, ×200). b Quantitative analysis of TH-positive areas in the renal cortex. c ELISA quantification of renal norepinephrine levels. B RDN facilitated UGE by regulating renal SGLT2 expression. a Representative images of SGLT2 immunofluorescence staining in the kidney (magnification, ×200). b WB analysis of protein levels of SGLT2 in the kidney. c Quantitative analysis of SGLT2 fluorescence intensity in the kidney. d The relative levels of SGLT2 calculated from the WB. e The 24-h urine volume of rats from three groups collected in the metabolic cage study. f Urinary glucose concentration of rats from three groups. (P < 0.05; n = 6, 9, and 10 in the control, DCM, and RDN groups, respectively; five sections were randomly selected per sample.) *P < 0.05 vs. the control group; #P < 0.05 vs. the DCM group. RDN renal denervation, DCM diabetic cardiomyopathy, TH tyrosine hydroxylase, UGE urinary glucose excretion, SGLT2 sodium-glucose cotransporter 2.

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