This may also be related to the significant reduction in NF-κB expression, inhibiting the formation or release of inflammatory mediators, and reducing nerve excitability, eliminating abnormal discharge after DZXXI treatment of cerebral ischemia and reperfusion in rats, thereby improving microcirculation, increasing oxygen supply to brain tissue, and reducing reperfusion injury after cerebral ischemia (Niu et al., 2007). This evidence concerns the gene NFKB1 and brain ischemia.