基础医学与临床 ›› 2007, Vol. 27 ›› Issue (12): 1360-1364.

• 研究论文 • 上一篇    下一篇

抗血管内皮生长因子抑制裸鼠异位子宫内膜生长

王含必 郎景和 冷金花 朱兰 刘珠凤 孙大为   

  1. 北京协和医院妇产科 北京协和医院妇产科 北京协和医院妇产科 北京协和医院妇产科 北京协和医院妇产科 北京协和医院妇产科
  • 收稿日期:2006-05-30 修回日期:2007-03-12 出版日期:2007-12-25 发布日期:2007-12-25
  • 通讯作者: 王含必

Anti-VEGF antibody restrains endometriotic-like lesions growth in the nude mouse model

Han-bi WANG, Jing-he LANG, Jin-hua LENG, Lan ZHU, Zhu-feng LIU, Da-wei SUN   

  1. Dept. Gynecology and Obstetrics, Peking Union Medical College Hospital, CAMS & PUMC
  • Received:2006-05-30 Revised:2007-03-12 Online:2007-12-25 Published:2007-12-25
  • Contact: Han-bi WANG,

摘要: 目的 构建子宫内膜异位种植裸鼠模型,在此基础上研究抗血管内皮生长因子(VEGF)抗体在治疗中的作用及机制。方法 将人子宫内膜组织种植到裸鼠体内,抗VEGF抗体作用于种植灶,进行分组对照研究。用TUNEL标记法检测细胞凋亡、PCNA检测细胞增殖和微血管密度(MVD)。结果 实验组细胞凋亡强度明显高于对照组,细胞增殖强度在各组间无明显差异。实验组人源性MVD和鼠源性MVD都明显低于对照组(p<0.05)。结论 抗VEGF抗体可能是通过促进子宫内膜细胞和血管内皮细胞的凋亡、抑制血管生成,继而抑制内膜异位种植生长,而对细胞增殖无明显抑制作用。

Abstract: Objective To establish the nude mouse model for in vivo research on endometriosis. We study the mechanism and effect of anti-vascular endothelial growth factor (VEGF) antibody treatment on the growth of established endometriotic-like lesions in the nude mouse model. Methods A model in which human endometrium is implanted into nude mice was used to test the effect of anti-VEGF antibody. The models were seperated into control groups and experimental groups (using anti-VEGF antibody). The TUNEL, PCNA and MVD were used to evaluate the effects of apoptosis, proliferation and angiogenesis. Results The explants in the control groups develop a rich blood supply that enables them to survive and grow than those in the experimental groups. The apoptosis level of experimental groups(non-endometriosis 5.83±1.03;endometriosis 6.06±0.77) were significantly higher than those of the control groups(non-endometriosis 4.80±0.77;endometriosis 4.74±0.86),p<0.05. The proliferation level was no difference in these groups. The MVD in the control groups (human non-endometriosis 12.80±4.60, endometriosis 13.15±5.66; mouse non-endometriosis 29.7±19.6, endometriosis 34.6±16.3) were higher than those in the experimental groups (human non-endometriosis 7.17±2.25; endometriosis 7.32±1.30; mouse non-endometriosis 11.2±6.2; endometriosis 15.6±6.8). The anti-VEGF antibody was used as accelerating apoptosis of the endometrial cells and vascular endothelium cells and no use for the proliferation. Conclusion In summary, anti-VEGF antibody effectively interfered with the maintenance and growth of endometriotic-like lesions by disrupting the vascular supply. This suggests that the anti-VEGF antibody may be provided a novel therapeutic approach for the treatment of endometriosis.