Empagliflozin ameliorates diabetic cardiomyopathy probably via activating AMPK/PGC-1α and inhibiting the RhoA/ROCK pathway

Figure 6 Relationship of empagliflozin with AMP-activated protein kinase, peroxisome proliferator-activated receptor-γ coactivator-1α, and the RhoA/ROCK pathway in cardiomyocytes in HG conditions in vitro. A-D: The phosphorylation of AMP-activated protein kinase and myosin phosphatase target subunit 1, as well as the protein expression of peroxisome proliferator-activated receptor-γ coactivator-1α were measured by Western blot in three groups; E: Sodium-glucose cotransporter (SGLT)1 and SGLT2 protein expression in cardiomyocytes. Bars indicate the mean ± SD from three independent experiments (n = 3). β-tubulin was set as a control for normalization. NG: Normal glucose; HG: High glucose; EM: Empagliflozin; CC: Compound C; FA: Fasudil; HG + Ad–PGC: Cells were transfected with PGC-1α-GFP-Ad. ^aP < 0.05 vs NG; ^bP < 0.05 vs HG; ^cP < 0.05 vs HG + EM.