Objective We aimed to evaluate the therapeutic effect of Bushen Wenyang Huayu Recipe (BWHR) on a rat model of endometriosis (EM) that involves kidney yang deficiency and blood stasis and determine whether its mechanism of action involves FoxO1-mediated autophagy. Methods Female-specific pathogen-free SD rats aged 8 ~ 10 weeks were randomly allocated to a sham surgery group, a model group, a high-dose BWHR group, a low-dose BWHR group, or a western medicine group (n= 20). A rat model of EM associated with kidney yang deficiency and blood stasis was established by autologous transplantation combined with an ice bath. After confirmation of the successful induction of EM, the high-dose and low-dose groups were administered BWHR, the western medicine group was administered gestrinone suspension, and the sham and model groups were administered the same volume of water by gavage for 3 weeks. Subsequently, the mechanical pain threshold of the rats was measured using a mechanical electronic pain meter, and organ indices were calculated. The histopathological changes in the eutopic endometrium and ectopic foci were evaluated on hematoxylin and eosin-stained sections. The expression of FoxO1, NF-κB, Beclin-1 and LC3 in eutopic endometrium and ectopic lesions was assessed using immunohistochemistry. The mRNA and protein expression of FoxO1, NF-κB, Beclin-1, LC3-I, and LC3-II was measured using Real time PCR and Western Blot, respectively. Results The protein and mRNA expression of FoxO1, NF-κB, Beclin- 1, LC3-I, and LC3-II was significantly higher in the model group than in the control group (P< 0. 05). However, the protein and mRNA expression of FoxO1, NF-κB, Beclin-1 and LC3 in eutopic endometrium and ectopic lesions in the high-dose and low-dose BWHR groups were significantly lower (P< 0. 05). Conclusions FoxO1, NF-κB, and the autophagy related factors Beclin-1 and LC3 may be involved in the development of EMs and have synergistic effects. BWHR may ameliorate EM by reducing the expression of FoxO1 and NF-κB, which inhibits autophagy.