Objective:To study the effects of brucine on vascular endothelial growth factor(VEGF)expression and microvessel density(MVD)in a nude mouse model of bone metastasis due to breast cancer,and to assess the possible antitumor mechanism of brucine.Methods:A syringe needle was used to directly inject 0.2 mL monoplast suspension(with 2×10~6 human breast cancer cells contained)into the bony femoral cortex of the right hind leg for modeling.Twenty-five nude mice were randomized into five groups and administered with an intraperitoneal injection of saline or drug for 8 consecutive days:model group(0.2 mL normal saline),low-dose brucine group(1.73 mg·kg~(-1)),medium-dose brucine group(3.45 mg·kg~(-1)),high-dose brucine group(6.90mg·kg~(-1),and thalidomide group(200 mg·kg~(-1)).Diet and activity were recorded,and the tumors were harvested 5 weeks later.The percentage of VEGF-positive cells was determined with hematoxylin and eosin staining and immunohistochemical staining,and MVD expression was determined by optical microscopy.Results: The VEGF expressions in brucine-or thalidomide-treated mice were significantly reduced as compared with mice in the model group(P<0.01).There were no significant difference between the high-dose brucine group and the thalidomide group(P>0.05).Significant difference was between the high-and low-dose brucine group (P<0.05).Further,VEGF expression was significantly increased in the low-and medium-close brucine groups compared with the thalidomide group(P<0.05).The MVD values in the three brucine and thalidomide groups were significantly lower than that in the model group(P<0.01).The MVD values in the medium-and high-dose brucine groups were not significantly different from those in the thalidomide group(P>0.05),while the MVD value showed a significant increase in the low-dose group compared with the thalidomide group(P<0.05).Conclusion:Brucine could inhibit the growth of breast cancer to bone metastases,possibly by inhibiting tumor angiogenesis. Objective: To study the effects of brucine on vascular endothelial growth factor (VEGF) expression and microvessel density (MVD) in a nude mouse model of bone metastasis due to breast cancer, and to assess the possible antitumor mechanism of brucine. Methods: A syringe needle was used to directly inject 0.2 mL monoplast suspension (with 2 × 10 ~ 6 human breast cancer cells contained) into the bony femoral cortex of the right hind leg for modeling.Twenty-five nude mice were randomized into five groups and administered with an intraperitoneal injection of saline or drug for 8 consecutive days: model group (0.2 mL normal saline), low-dose brucine group (1.73 mg · kg -1), medium-dose brucine group (3.45 mg · kg -1 1), high-dose brucine group (6.90 mg · kg -1, and thalidomide group (200 mg · kg -1)). Diet and activity were recorded, and the tumors were harvested 5 weeks later. The percentage of VEGF-positive cells was determined with hematoxylin and eosin staining and immunohistochemical staining, and MVD expression was determined by optical microscopy. Results: The VEGF expressions in brucine-or thalidomide-treated mice were significantly reduced as compared with mice in the model group (P <0.01). Everyone no significant difference between the high-dose brucine group and the thalidomide group (P> 0.05) .Significant difference was between the high-and low-dose brucine groups (P <0.05) .Further, VEGF expression was significantly increased in the low-and medium- close brucine groups compared with the thalidomide group ( The MVD values ​​in the three brucine and thalidomide groups were significantly lower than that in the model group (P <0.01). The MVD values ​​in the medium-and high-dose brucine groups were not significantly different from those in The thalidomide group (P> 0.05), while the MVD value showed a significant increase in the low-dose group compared with the thalidomide group (P <0.05) .Conclusion: Brucine could inhibit the growth of breast cancer to bone metastases, possibly by inhibiting tumor angiogenesi s.