AIM: This work aims to investigate the treatment effect of endostatin (ES) in the nude mouse model with endometriosis (EMs). MATERIALS AND METHODS: Recombinant adenovirus Ad-ES carrying ES gene was constructed. Apoptosis of ECV-304 cell induced by Ad-ES was observed. The nude mouse model with EMs was established by subcutaneous implantation. After the local focus was injected with the Ad-ES, the Ad-Track or the physiologic saline, respectively, the morphological features of ectopic focuses were observed under microscopy. The microvessel densities (MVD) and the apoptosis were detected. RESULTS: The recombinant Ad-ES was successfully constructed. Apoptosis of ECV 304 cells could be induced by Ad-ES. The nude mouse model with EMs was successfully established by subcutaneous implantation. There were statistical differences in the volumes of endometriotic lesions and MVD after treatment by Ad-ES compared with those in the other two control groups (p < 0.05). Apoptosis of the cells were significantly increased in the group of treatment by Ad-ES compared with those of the two control groups. CONCLUSION: ES could induce ECV 304 cells to apoptosis and inhibit the growth ofendometrium in the nude mouse model. The findings suggest that antiangiopoiesis may be used as a promising therapy for the treatment of EMs.
AIM: This work aims to investigate the treatment effect of endostatin (ES) in the nude mouse model with endometriosis (EMs). MATERIALS AND METHODS: Recombinant adenovirus Ad-ES carrying ES gene was constructed. Apoptosis of ECV-304 cell induced by Ad-ES was observed. The nude mouse model with EMs was established by subcutaneous implantation. After the local focus was injected with the Ad-ES, the Ad-Track or the physiologic saline, respectively, the morphological features of ectopic focuses were observed under microscopy. The microvessel densities (MVD) and the apoptosis were detected. RESULTS: The recombinant Ad-ES was successfully constructed. Apoptosis of ECV 304 cells could be induced by Ad-ES. The nude mouse model with EMs was successfully established by subcutaneous implantation. There were statistical differences in the volumes of endometriotic lesions and MVD after treatment by Ad-ES compared with those in the other two control groups (p < 0.05). Apoptosis of the cells were significantly increased in the group of treatment by Ad-ES compared with those of the two control groups. CONCLUSION: ES could induce ECV 304 cells to apoptosis and inhibit the growth ofendometrium in the nude mouse model. The findings suggest that antiangiopoiesis may be used as a promising therapy for the treatment of EMs.