First, on a cell model, primary cortical neurons were used to determine the safe dose of ginsenoside by performing toxicity assays with different concentration gradients of ginsenoside using MTT assay; Then pharmacodynamic screening was performed using primary cortical neuron oxygen-glucose deprivation reperfusion (OGD/R), and primary cortical neurons cultured to day 7 were replaced with sugar-free DMEM after drug preadministration for 2h.Then the neurons were placed in a hypoxic chamber containing 95% N2 and 5% CO2 for 4 h, and after that they were switched to the normal medium containing ginsenoside, and the cell viability was examined by MTT assay after re-sugar and reoxygenation for 24h to screen for the protective activities of ginsenoside . In the middle cerebral artery ischemia-reperfusion (tMCAO) model, the ginsenoside was given by gavage twice daily for 3 days after modelling, using 7- to 8-week-old male C57BL/6 mice, and the protective effects on cerebral ischemic stroke were evaluated by TTC staining after 3 days. Behavioral changes of tMCAO mice was assessed using the mNSS neurological function score. At the cellular level, MTT results showed that ginsenoside was not toxic to primary cortical neurons at doses of 80 μM and below, and in the OGD/R model, ginsenoside was found to have ameliorative effects on OGD/R-induced primary cortical neuronal cell injury, In the tMCAO model, TTC results showed that ginsenoside (5 and 10 mg/kg) was effective in reducing the infarct volume in tMCAO mice, and mNSS results showed that ginsenoside could improve the neurological function of tMCAO mice.