This study aimed to demonstrate the mechanism of bevacizumab in inhibiting angiogenesis in mice with ovarian cancer (OC) by regulating JAK2/STAT3 pathway. Forty healthy femaleBALB/C nude mice were randomly assigned to control, model, erlotinib, and bevacizumab groups. Control group received no treatment. Model group received subcutaneous injection in the left axillary region to establish the OC model and received an equal volume of normal saline. Bevacizumab group underwent the same model - establishment procedure and then received 5mg/kg bevacizumab intervention. Erlotinib group also underwent model establishment and received 30mg/kg erlotinib intervention. Tumor tissue massand tumor inhibition rate were recorded. The tumor pathological changes were analyzedby hematoxylin-eosin (HE)staining. The microvessel density (MVD) and vascular endothelial growth factor (VEGF) protein expressionin tumor tissues were subjected to detection by immunohistochemistry. The expression of JAK2,STAT3,andVEGF in tumor tissues was analyzed using RT-qPCRand western blotting.Compared with the model group, tumor volume and weight of OC in erlotinib group and bevacizumab group of mice were visibly reduced. MVD, JAK2, STAT3, and VEGF in model, erlotinib, and bevacizumab groupsof mice were increased versus control, while those were decreased in erlotinib and bevacizumab groups of mice versus model group (P<0.05).Bevacizumabeffectively suppressing tumor growthbyreducing tumor angiogenesis and reducing the expression of key molecules ofJAK2/STAT3pathway in mice.