In present study, we first demonstrated that: (1) hyperglycemia can aggravate the downregulation of sirt3 in animal models of ICH; (2) HKL ameliorates oxidative stress and mitochondrial dysfunction via a sirt3-dependent manner after hyperglycemic ICH; and (3) Sirt3 activation could also decrease NLRP3 and IL-1β levels through deacetylating SOD2 and scavenging ROS. This evidence concerns the gene SOD2 and Hyperglycemia.