We found that UTI improves neurological dysfunction after ICH, alleviates brain damage in a mouse ICH model, relieves neuroinflammation after ICH and then decreases inflammatory damage in the brain, prevents oxidative stress after ICH and alleviates neuronal death, and the antiapoptotic and antioxidative stress effects of UTI may be related to the ROS/MAPK/Nrf2 signaling pathway (Fig. 7). The gene discussed is NFE2L2; the disease is bacterial urinary tract infection.