Additionally, BPS induces neurotoxicity in IMR-32 cells by increasing MDA content, reducing SOD activity, and producing excessive ROS [10,32]; studies have shown that PUE treatment can increase SOD activity, alleviate oxidative stress, and significantly inhibit ROS production in mice with subarachnoid hemorrhage (SAH) [26]. This evidence concerns the gene SOD1 and subarachnoid hemorrhage.