Objective To observe the effects of Wenjingzhitong decoction (WJZT) on expression of molecules in the AKT/ mTOR pathway secreted by eutopic and ectopic endometria of endometriosis (EMS) rats. Methods Autologous transplantation of the uterine was used to establish the rat model of endometriosis. Seventy-five endometriosis rats were randomly divided into five groups: WJZT high-, medium-, and low-dose groups, and Nemestran and model control groups.Sham surgery rats were used for the normal control group. The WJZT high-, medium-, and low-dose groups were treated with different concentrations of Wenjingzhitong decoction, respectively. Nemestran (gestrinone) capsule was administered to the Nemestran group, and 0. 9% NaCl was administered to model and normal groups. AKT and mTOR mRNA and protein expressions were detected by real-time PCR and immunohistochemistry, respectively. Serum levels of vascular endothelial growth factor (VEGF) were detected by ELISA. Results Compared with the normal control group, protein and mRNA expressions of AKT and mTOR in eutopic and ectopic endometria was increased in the model groups ( P < 0. 01). AKT and mTOR mRNA levels in eutopic and ectopic endometria of the WJZT high-dose group and Nemestran (gestrinone) group was lower than that in the model control group ( P < 0. 05). Compared with the normal control group, serum VEGF level in the EMS model groups was increased ( P < 0. 01). Compared with the model control group, serum VEGF levels in the WJZT high- and low- dose groups and the Nemestran group were decreased ( P < 0. 01), and serum VEGF level in the WJZT medium-dose group was also decreased ( P < 0. 05). Conclusions Endometriosis is associated with the AKT/ mTOR signaling pathway and the levels of VEGF. WJZT inhibits AKT/ mTOR and regulates the level of VEGF. Therefore, WJZT can inhibit cell adhesion, invasion, and angiogenesis in the ectopic endometrium.