Objective To establish an efficient and stable model of pelvic inflammatory disease in rats via a non-surgical method, and to evaluate its application in pharmacodynamic testing. Methods Female Sprague-Dawley rats were divided randomly into the following groups: control group; model group with phenol for 7 d; model group with phenol for 10 d; treatment group modeled with phenol; model group with low concentration of bacteria; model group with high concentration of bacteria; and treatment group modeled with bacteria. Rats in the model and treatment groups were injected with 25% phenol gel and 2×10⁷or 2×10⁸ Escherichia coli and Staphylococcus aureus mixture via a non-surgical method, to construct a rat model of pelvic inflammatory disease. Rats in the treatment groups received the Chinese patent medicine Jingangteng capsules by gavage, and rats in the control group received the same volume of solvent solution. The health status, weight changes, and uterine appearance were monitored and the uterine coefficient was calculated. Pathological changes in the uterus and fallopian tubes, endometrial thickness, and number of glands were detected by hematoxylin and eosin staining. Serum levels of interleukin (IL)-1β, IL-6, and tumor necrosis factor (TNF)-α were detected by enzyme-linked immunosorbent assay. Protein expression of the macrophage marker CD68 was detected by immunofluorescence. Expression of Toll-like receptor 4 (TLR4)/nuclear factor (NF)-κB pathway-related proteins in the uterus was detected by Western blot. Results The mortality rate in the model group was only 5%. Compared with the control group, model rats showed decreased body weight, increased uterine coefficient, pathological changes in the uterus and Fallopian tubes, thinner endometrium, fewer glands, significantly higher serum levels of IL-1β, IL-6, and TNF-α and more macrophages in the uterine tissue, and activation of the TLR4/NF-κB signaling pathway. The 7 d phenol and low-concentration bacterial solution models were judged to be mild pelvic inflammatory disease models, and the 10 d phenol and high-concentration bacterial solution models were considered severe pelvic inflammatory disease models. Treatment with Jingangteng capsules relieved the pathological symptoms in the uterus and fallopian tubes, in line with the efficacy evaluation of clinical pelvic inflammatory disease. Conclusions We established rat models of pelvic inflammatory disease using phenol and a mixed bacterial solution via a non-surgical method, to simulate the different pathological states of pelvic inflammatory disease caused by different factors. These models will be suitable for evaluating drug efficacy and elucidating the pathological mechanism of pelvic inflammatory disease.