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

Figure 5 Effects of empagliflozin, fasudil, and overexpression of peroxisome proliferator-activated receptor-γ coactivator-1α on high glucose-induced mitochondrial injury and oxidative stress in vitro. A: Levels of intracellular high glucose; B and C: Changes in mitochondrial membrane potential; D: Cellular ATP production; E: Cellular superoxide dismutase activity. Bars indicate the mean ± SD from three independent experiments (n = 3). ROS: Reactive oxygen species; MMP: Mitochondrial membrane potential; SOD: Superoxide dismutase; 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.