This study aims to investigate the anti-hypoxic effect of compound ginseng (CGS) and its molecular mechanism.The atmospheric pressure hypoxia tolerance model,the sodium nitrite poisoning model,the acute cerebral ischemia model and the whole heart ischemia-hypoxia model were constructed,and the effects of CGS on survival time,gasping time,gasping frequency,malondialdehyde (MDA) content,superoxide dismutase (SOD) activity,glutathione peroxidase (GSH-Px) activity,lactic dehydrogenase (LDH) activity,and creatine kinase (CK) activity were oberved.Network pharmacology was utilized to predict the anti-hypoxia related mechanism of CGS,and molecular docking method was used to verify the affinity between the active ingredients of CGS and the body targets obtained from network pharmacology screening,and to detect the mRNA expression of hypoxia inducible factor-1α (HIF-1α) and vascular endothelial growth factor (VEGF) in mice.The results showed that CGS significantly prolonged the survival time of mice in the atmospheric pressure hypoxia tolerance experiment,sodium nitrite intoxication experiment and whole heart ischemia-hypoxia experiment,as well as gasping time and gasping frequency in the acute cerebral ischemia experiment;CGS was able to reduce the serum levels of MDA,LDH,and CK viability,and elevate the activities of SOD and GSH-Px in mice.Network pharmacology was used to predict 226 anti-hypoxia pathways of CGS,among which the key pathway was the HIF-1α pathway.the results of the confined hypoxia experiments confirmed that CGS could significantly elevate the expression of HIF-1α and down-regulate the expression of VEGF.In conclusion,CGS has the anti-hypoxia effect,and its action may be related to the activation of the HIF-1α/VEGF pathway,which improves the oxygen-carrying capacity of the blood and oxygen utilization,and enhances the antioxidant activity.