The Neuroprotective Effect of Shenmai Injection on Oxidative Stress Injury in PC12 Cells Based on Network Pharmacology

Abstract

Background. Shenmai injection (SMI) has been used in the treatment of cerebrovascular diseases and cardiovascular diseases. However, the underlying mechanism of SMI for neuroprotection after acute ischemic stroke (AIS) remains unclear. This study aimed to explore the potential molecular mechanism of SMI in treating reperfusion injury after AIS and its protective effect on PC12 cells against oxidative stress through in vitro experiments based on network pharmacological predictions. Methods. The network pharmacology method was used to collect the compounds in SMI and AIS damage targets, construct the “drug-disease” target interaction network diagram, screen the core targets, and predict the potential mechanism of SMI treatment of AIS. In addition, the oxidative stress model of PC12 cells was induced by H2O2 to evaluate the neuroprotective effect and predictive mechanism of SMI on PC12 cells. Results. A component-targeted disease and functional pathway network showed that 24 components from SMI regulated 77 common targets shared by SMI and AIS. In PC12 cells damaged by H2O2, SMI increased cell survival, alleviated oxidative stress injury, prevented cell apoptosis, and increased the expression of APJ, AMPK, and p-GSK-3β. After Si-APJ silenced APJ expression, the above protective effect of SMI was significantly weakened. Conclusion. SMI is characterized by multiple components, multiple targets, and multiple pathways and inhibits oxidative stress and alleviates nerve injury induced by H2O2 through regulating the APJ/AMPK/GSK-3β pathway.