Figure 3.

Allopurinol treatment prevented HG‐induced increased cell size and elevated oxidative stress, which can be cancelled by gene silence of Nrf2 in H9C2 cells. H9C2 cardiomyocytes were pretreated with Nrf2 siRNA and control siRNA and then treated with control medium with normal glucose (NG, 5.5 mmol/L glucose) or HG (25 mmol/L glucose) for 48 h; subgroups were treated with ALP for 48 h at the meantime before sample collection. A, B, H9C2 cell size visualization (400 magnification, 50 µm) and quantitation. D, E, Cellular reactive oxygen species production assessed by dihydroethidium (DHE) staining in H9C2 cell (The scale bar in the figure represents 400 µm). C, H9C2 cardiomyocyte viability assessed by CCK8 agent. F, Cardiomyocyte death assessed by lactate dehydrogenase (LDH) release. G, H, Apoptosis of H9C2 myocytes assessed by TUNEL staining (The scale bar in the figure represents 400 µm). Data are mean ± SEM of two independent experiments each performed in triplicate, *P < .05. vs NG; ^# P < .05 vs HG; ^$ P < .05 vs HA; ^& P < .05 vs Nrf2