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

Figure 4 Effects of empagliflozin, fasudil, and overexpression of peroxisome proliferator-activated receptor-γ coactivator-1α on apoptotic genes and related proteins in vitro. A and B: Bax and Bcl-2 mRNA expression was quantified using real-time quantitative PCR in cardiomyocytes; C: Protein expression of active caspase-3 measured by Western blot. 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 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.