SOD1 and infarction: In this study, we first confirmed that HKL inhibited ROS production and MDA generation, increased the ROS scavenging activities of SOD, and depressed the expressions of gp91phox and apoptotic signaling in diabetic heart following MI/R injury, therefore attenuating myocardial oxidative stress, reducing cardiomyocyte apoptosis, and ultimately decreasing infarction size and ameliorated cardiac dysfunction.