To investigate the changes of NF-κB, inflammatory factors, and metabolic factors of model rats with endometriosis, and to study their influences on cell invasion and apoptosis. Methods: SD rats were randomly divided into group A (control group), group B (model group), group C (positive group), and group D (PDTC group). The model rats with endometriosis in group A, B, and C were built by autotransplantation. The model rats in group C were injected intraperitoneally with 0.25 mg/kg/d of gestrinone for 21 days, the model rats in group D were injected intraperitoneally with a PDTC solution of 100 mg/kg/d for 21 days, and the model rats in group A and B were injected intraperitoneally with equal doses of normal saline for 21 days. The NF-κB activity was detected by western blot, the TNFα, IL-6, IL-1β, ICAM-1, and VCAM-1 were analyzed by ELISA, the Transwell was used to analyze the invasion of intimal cells, and the TUNEL staining was used to detect the intimal cell apoptosis. Results：The activity of NF-κB and the levels of TNF-α, IL-6, IL-1β, ICAM-1, and VCAM-1 of the endometrial cells of rats in group B were significant higher than those of rats in group A, and those of rats in group C and D were significant lower than those of rats in group B (P＜0.05). Transwell showed that the cell invasion of rats in group B was significant higher than that of rats in group A (P＜0.05), while that of rats in group C and D was significant lower than that of rats in group B (all P＜0.05). TUNEL staining showed that the apoptosis index of rats in group B was significant lower than that of rats in group A (P＜0.05), and which of rats in group C and D was significant lower than that of rats in group B (all P＜0.05). Conclusion: The activity of NF-κB of model rats with endometriosis increases significantly, which maybe promote the invasion of endometrial cells and inhibite their apoptosis by up regulating the expression of inflammatory and adhesion factors.