Objective: To explore the protective effect and mechanism of butylphthalide on ischemic brain injury in vitro and in vivo.

Method: 24 SD rats were randomly divided into control group, model group, low-dose butylphthalide group, and high-dose butylphthalide group in vivo experiment, with 6 rats in each group. The drug was administered by gavage once a day for 1 month. The animal model of permanent middle cerebral artery occlusion was established by electrocoagulation, and the administration was continued until the tenth day after modeling, and detected relevant indicators. The primary neuron cells were randomly divided into control group, model group and experimental group in vitro experiment, and subsequently established a hypoxia and hypoglycemia/reoxygenation and complex glucose model, and detected related indicators

Results: In vivo experiment, on the tenth day after modeling, compared with the controlgroup, the model group had significant neurological deficits and a larger cerebral infarction volume, and the content of TNF-a and IL-1β increased significantly (P<0.01)and the level of TARF6 protein increased and Nrf2 protein decreased significantly.However, the injury in the high-dose butylphthalide group was reversed. In vitro experiment, compared with the control group, the content of TNF-a , lL-β and ROS in the model group was significantly increased, and the SOD activity was significantly decreased the TRAF6 protein expression was increased, and the Nrf2 expression was decreased. The injury in the butylphthalide group was relieved.

Conclusion: By inhibiting infammation and oxidative stress, butylphthalide plays a protective role in ischemic brain injury.