Objective To explore the effect of Dingkun pill on the PI3K/ AKT/ mTOR signaling pathway in rats with endometriosis (EM). Methods EM rat models were established by heterotopic transplantation of endometrial tissue and randomly divided into five groups: model group (M group), Dingkun pill low (1. 13 g/ kg) dose group (DKP-L group), Dingkun pill medium (2. 26 g/ kg) dose group (DKP-M group), Dingkun pill high (4. 52 g/ kg) dose group (DKP-H group) and gestrinone (60 mg/ kg) group (GES group) with 12 rats in each group. The abdomen was opened without transplantation of ectopic endometrial tissue in another 12 normal SD rats as sham operation group (Sham group). The rats were sacrificed after drug treatments, The mass and volume of ectopic endometrium were measured. The microvessel density (CD31-positive rate) and expression of VEGF and MMP-9 in rat ectopic endometrial tissue were assessed by immunohistochemical staining. Rat serum VEGF, MMP-9, iNOS and TNF-α levels were measured by enzymelinked immunosorbent assays. Expression of PI3K/ AKT/ mTOR pathway-related proteins in rat ectopic endometrial tissue was detected by Western blot. Results Compared with those in the sham group, the microvessel density, VEGF and MMP-9 expression, serum VEGF, MMP-9, iNOS and TNF-α levels, p-PI3K/ PI3K, p-AKT/ AKT and p-mTOR/ mTOR in ectopic endometrial tissue were significantly increased in the M group (P<0. 05). Compared with the findings in the M group, the ectopic endometrial volume, weight of the ectopic lesion, microvessel density of the ectopic endometrial tissue, VEGF and MMP-9 expression, serum VEGF, MMP-9, iNOS and TNF-α levels, p-PI3K/ PI3K, p-AKT/ AKT, and pmTOR/ mTOR in ectopic endometrial tissue were all decreased in the DKP-L, DKP-M, DKP-H groups, and dosedependent effects were observed in Dingkun pill low dose, Dingkun pill medium dose, and Dingkun pill high dose groups(P<0. 05). Compared with DKP-H group and GES group, no significant difference was found in the indicators (P>0. 05). Conclusions Dingkun Dan reduces inflammation and inhibits ectopic endometrial growth in EM rats, which may be achieved by blocking the PI3K/ AKT/ mTOR signal pathway.