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. 2010 Feb;176(2):850–860. doi: 10.2353/ajpath.2010.090551

Figure 7.

Figure 7

Inhibition of PGE2 production increases the phagocytic ability of macrophages and reduces endometriosis formation in vivo (n=10 animals per group). A: Concentrations of PGE2 in the peritoneal fluid of mice without (disease-free) or with surgery-induced endometriosis. Mice with endometriosis were further divided into four groups and treated with vehicle (Veh), COX-1 inhibitor (ketorolac, Ke, 10 mg/kg body weight), COX-2 inhibitor (NS398, 10 mg/kg body weight), or COX-1/-2 inhibitor (indomethacin, Indo, 10 mg/kg body weight) for 4 weeks. B: Mean and SD of the number of endometriotic-like lesions in mice treated with COX inhibitors. C: Mean and SD of total wet-weight of endometriotic lesions in mice treated as described above. D: CD36 expression in mouse peritoneal macrophages after surgery-induced endometriosis and drug treatment. E: Representative flow cytometric results of phagocytic ability of freshly isolated peritoneal macrophages after surgery-induced endometriosis and drug treatment. F: Mean and SD of the percent of phagocytic macrophages (lower panel) and mean phagocytosis index (upper panel) in peritoneal macrophages freshly isolated from surgery-induced endometriotic mice. M0: no bead was ingested; M1: with at least one bead ingested *P < 0.05, **P < 0.01, ***P < 0.001, as compared with control.