Ornidazole Reduces the Progression of Endometriosis in a Rat Model

OBJECTIVE: The aim of this study was to investigate the effectiveness of ornidazole in inhibiting the progression of endometriosis in a rat model. DESIGN: This was an in vivo experiment, including the ornidazole group (n = 16) and a control group (n = 14). Rats were provided with free access to water containing ornidazole (1 g/L) or drinking water only for 14 days. MATERIALS AND METHODS: Surgical induction of endometriosis was performed in Sprague Dawley rats via autologous endometrial transplantation. Rats were provided with free access to water containing ornidazole (1 g/L) or drinking water only for 14 days. Once the rats were euthanized (ornidazole group, n = 16; control group, n = 14), histological signatures and the volumes of endometriosis lesions were assessed. Cells positive for the inflammatory cytokines interleukin (IL)-1β, IL-6, and tumor necrosis factor (TNF)-α were counted. Angiogenesis was identified by assessing vascular endothelial growth factor (VEGF) and microvessel density. RESULTS: The median lesion volume was lower in the ornidazole group (20.2 mm(3); range, 5.7–53.3 mm(3)) than in the control group (81.3 mm(3); range, 32.8–122.2 mm(3); p = 0.007). Median IL-1β cell counts were 5.3 (range, 4.5–6.4) for ornidazole and 11.7 (range, 9.4–15.4) for control (p < 0.001). Mean IL-6 cell counts were 5.6 ± 1.8 for ornidazole and 11.3 ± 4.1 for control (p < 0.001). Median TNF-α cell counts were 5.7 (range, 4.5–7.2) for ornidazole and 12.1 (range, 10.0–15.9) for control (p < 0.001). Median VEGF cell counts were 8.1 (range, 6.5–11.4) for ornidazole and 18.3 (range, 14.2–21.0) for control (p = 0.001). Median microvessel density values were 11.3/HPF (range, 7.7–21.8) for ornidazole and 28.7/HPF (range, 13.1–48.2) for control (p = 0.012). LIMITATIONS: This study is a short period and small sample size experiment. In this study, multiple drug concentrations were not used. We did not use in vitro models to assess the anti-inflammatory and antiangiogenic effects of ornidazole on endometriosis, and the specific anti-inflammatory and antiangiogenic mechanisms associated with ornidazole need to be further investigated. CONCLUSION: Ornidazole restricts the growth of endometriosis in rats, possibly by exerting anti-inflammatory and antiangiogenic effects.