FIGURE 3.

Nox2 gene knockdown attenuated post‐hypoxic oxidative stress and programmed cell death in cardiomyocytes exposed to high glucose. A, LDH release during hypoxia reoxygenation (H/R) in normal (NG) and (HG), with or without siRNA‐mediated knockdown of Nox2; B, WB band showing protein expression of Nox2, NLRP3, Cleaved caspase‐3, GPX4 and GAPDH; C, the change in protein expression of Nox2 during H/R in NG and HG, with or without siRNA Nox2; D, The change in protein expression of NLRP3 during H/R in NG and HG, with or without siRNA Nox2; E, The change in protein expression of cleaved caspase‐3 during H/R in NG and HG, with or without siRNA Nox2; F, The change in protein expression of GPX4 during H/R in NG and HG, with or without siRNA Nox2. In the HG group, H9C2 cells were subjected 30 mmol/L glucose treatment for 48 h, H/R was achieved by 6 h hypoxia exposure and 12 h reperfusion. Data are expressed as mean ± SEM of two independent experiments, each performed in triplicates. n = 6 per group. *P < 0.05, **P < 0.01