CONICET | Buscador de Institutos y Recursos Humanos

One of the main factors involved in the neovascularization of the ectopic endometrial tissue in endometriosis (EDT) is VEGF, which is produced by the endometrial tissue as well as by the peritoneal macrophages. In addition, it is known that VEGF levels in the peritoneal fluid (PF) and in lesions from patients with EDT are increased compared to controls and eutopic endometrium respectively. The aim of this work was to evaluate the effect of two VEGF inhibitors: Bevacizumab, an anti-VEGF humanized antibody; and a polyclonal anti-murine VEGF antibody, on EL development and VEGF levels in the PF in vivo, in a murine model of EDT. After fifteen days of having induced EDT, treatments began according to the following scheme: Bevacizumab group: intraperitoneal (i.p.) injection every three days of 5mg/kg of Bevacizumab (in physiologic solution); anti-murine VEGF group: one i.p. injection per week of 5mg/kg polyclonal antibody (in PBS); and control groups, received injections of physiologic solution or PBS the same days. By the second week of treatment, animals were sacrificed, the EL volume was determined and the PF was collected to assess VEGF levels by ELISA. Treatment with Bevacizumab significantly reduced the mean volume of the EL developed per animal (p<0.05 vs Control), as well as the peritoneal VEGF levels (p<0.05 vs Control). However, there were no differences in any of these parameters after the anti-murine VEGF treatment. On the other hand, there was no significant difference in the number of lesions developed per animal with any treatment. Our results suggest that Bevacizumab reduces the size rather than the number of developed lesions. Furthermore, it has been shown that the antibody reduced peritoneal VEGF levels in the EDT murine model.