objective based on the network pharmacology and in vivo experiments to explore the evening primrose oil (EPO) on polycystic ovary syndrome (PCOS), the improvement of rat aortic endothelial damage mechanism. Methods Network pharmacology was used to predict the potential targets of EPO to improve aortic endothelial injury in PCOS rats, and the selected core targets and RAS pathway were verified by experiments. Fifty-eight female SD rats were randomly divided into blank group (10) and model group (48). The blank group was given normal diet, and the model group was given high-fat diet for 8 weeks. At the 6th week, the PCOS model was prepared by inadministration of letrozole (1mg/kg/d) for 21 days. After blood is taken from the tail vein was taken after modeling, serum was collected to detect hormone levels, and the model rats were randomly divided into 4 groups and given inadministration of corresponding drugs for 6 weeks. The blood, blood vessels and ovaries of the rats were collected after administration. hematoxylin-eosin (HE) was hematoxylin-eosin (HE) to observe the tissue morphology, and ELISA was used to detect the levels of luteinizing hormone (LH), testosterone (T), follicle-stimulating hormone (FSH), endothelin (ET-1) and tumor necrosis factor (TNF-α) in serum. The levels of nitric oxide (NO) in serum of rats were determined by spectrophotometry. Protein expression levels of core targets and RAS pathway-related factors were assessed by Western Blotting and Immunohistochemistry (IHC). Results 25 intersection targets of EPO and PCOS were identified by network pharmacological analysis. KEGG results showed that EPO improved vascular injury in PCOS rats through multiple pathways, including Renin-angiotensin signaling (RAS). The results showed as follows: After EPO treatment, compared with the model group, ELISA results showed that the contents of ET-1, FSH, LH and T in serum of the treatment group were decreased, and the differences were statistically significant(P<0.05); Results: After treatment, the expressions of Ang I, VEGF-B, AT2R, ET-1 and TNF-α proteins in aorta were significantly decreased(P<0.05), while the expressions of Ang II, CD31 and e NOS proteins were significantly increased, with statistical significance(P<0.05). Conclusion In summary, EPO may ameliorate vascular endothelial injury in PCOS model rats by inhibiting RAS signaling pathway ACE/Ang II/AT1 axis overactivation.