摘要
目的:探讨内皮抑素对裸鼠子宫内膜异位病灶中血管生成素2(Ang-2)/酪氨酸蛋白激酶受体2(Tie-2)系统表达的影响。方法:采用腹膜种植方法建立子宫内膜异位症(EMs)裸鼠模型共60只。造模1周后,随机分成内皮抑素组、空病毒组和磷酸盐缓冲液(PBS)对照3组,每组各20只,观察各组镜下子宫内膜组织学变化,并采用免疫组化法检测各组异位内膜组织Ang-2及Tie-2的表达情况。结果:成功建立裸鼠EMs模型。空病毒组和PBS组腺体增生明显,间质血管丰富;内皮抑素组腺体萎缩,间质血管减少。Ang-2、Tie-2均在子宫内膜腺上皮细胞、间质细胞中表达,定位于细胞质。Ang-2在内皮抑素组的阳性率(40%)显著低于空病毒组(75%)和PBS组(80%)(均P<0.05);Tie-2在内皮抑素组的阳性率(45%)显著低于空病毒组(80%)和PBS组(85%)(均P<0.05)。结论:内皮抑素对裸鼠EMs模型异位病灶中Ang-2/Tie-2血管生成途径有抑制作用,为其抗血管生成治疗EMs的临床应用奠定基础。
Objective：To investigate the effects of endostatin on Ang-2/Tie-2 system in ectopic lesion.Methods：Thirty mice of endometriosis model （EM） were established by peritoneum planted.After 1 week of transplantation,model mice were randomly divided into three groups including rAAV2-hEndostatin-EGFP group （n=20）,rAAV2-EGFP group （n=20） and PBS control group （n=20）.The histology changes were examined in the three groups.The expressions of Ang-2 and Tie-2 were examined by immunohistochemistry.Results：The EM model mice were established successfully.The gland proliferation was obvious in the two control groups.The mesenchymal blood vessel was rich.But there were gland atrophy and blood vessel reducing in endostatin group.There were expressions of Ang-2 and Tie-2 in the cytoplasm of endothelium,epithelial glands and stroma.The positive rate of Ang-2 expression was 40%in endostatin group,much lower than that in other two groups （75% and 80%,P﹤0.05）.The positive rate of Tie-2 expression was 45% in endostatin group,which was also lower than that in other two groups （80% and 85%,P0.05）.Conclusion：Endostatin can effectively interfere angiogenesis process of Ang-2/Tie-2,which lays the foundation for clinical therapy by anti-angiogenesis.
出处
《天津医药》
CAS
北大核心
2010年第2期124-126,163,共4页
Tianjin Medical Journal
基金
天津市科委基金资助项目(项目编号:06YFJMJC08800)
