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

Figure 3 Effects of empagliflozin, fasudil, and overexpression of peroxisome proliferator-activated receptor-γ coactivator-1α on high glucose-induced cardiomyocyte apoptosis in vitro. A: Effects of different concentrations of empagliflozin on viability of cardiomyocytes exposed to high glucose (HG); B and C: Cardiomyocyte apoptosis measured by flow cytometry; D: TdT-mediated dUTP-biotin nick end labeling staining of cardiomyocytes in each group. Bars indicate the mean ± SD from three independent experiments (n = 3). NG: Normal glucose; HG: High glucose; EM: Empagliflozin; CC: Compound C; FA: Fasudil; HG + Ad–PGC: Cells were transfected with peroxisome proliferator-activated receptor-γ coactivator-1α-GFP-Ad; HG + Ad-GFP: Cells transfected with GFP-Ad. ^aP < 0.05 vs NG; ^bP < 0.05 vs HG; ^cP < 0.05 vs HG + EM.