Genistein does not affect vascularization and blood perfusion of endometriotic lesions and ovarian follicles in dorsal skinfold chambers of Syrian golden hamsters.

Genistein has previously been shown to cause regression of endometriotic lesions. In the current study, we investigated whether this observation is due to the antiangiogenic activity of genistein. Endometrial fragments and ovarian follicles were transplanted into dorsal skinfold chambers of hamsters, which were treated with genistein (50 and 200 mg/kg) or vehicle (control). Vascularization and blood perfusion of the grafts was analyzed over 14 days using intravital fluorescence microscopy and histology. Genistein inhibited angiogenesis neither in endometriotic lesions nor in ovarian follicles. This was indicated by a final microvessel density of the grafts, which was comparable to that of controls. Blood perfusion was not affected by genistein treatment. At day 14 after transplantation, the grafts of genistein- and vehicle-treated animals exhibited a histomorphology, which was typical for well-vascularized endometriotic lesions and ovarian follicles without any signs of regression. Thus, genistein may not be considered for the development of antiangiogenic treatment strategies in the therapy of endometriosis.