Similar results to this research were observed in the study by Yang BB et al. They constructed an acute cerebral infarction model in which AST pretreatment increased the Nrf2 and HO-1 proteins expression, and the levels of CAT, SOD, and GPX, indicating that AST enhanced neurological function meaningfully in rats through activating Nrf2/HO-1, reducing head cell apoptosis, and boosting antioxidant capacity [44]. Here, SOD1 is linked to cerebral infarction.