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目的探讨血管生成素-2(angiopoietin-2,Ang-2)在子宫内膜异位症(EMs)发生、发展中的作用以及促性腺激素释放激素类似物(GnRHa)对EMs在位内膜、异位内膜中Ang-2表达的影响。方法选择25例卵巢子宫内膜异位症(OEMs)病人作为未用药组,23例OEMs病人术前使用GnRHa 3个疗程,28例同期非内膜疾病妇女作为对照组。均留取子宫内膜,使用免疫组化染色方法检测Ang-2在OEMs用药及未用药组异位、在位子宫内膜及对照组正常子宫内膜中的表达。结果 Ang-2蛋白主要定位于子宫内膜腺上皮细胞的胞浆中。未用药组:Ang-2在OEMs组在位子宫内膜组织中的阳性表达率为80.00%,显著高于异位内膜(52.00%)和对照组(21.48%)(P<0.05);异位内膜组阳性表达率为52.00%,显著高于对照组(21.48%)(P<0.05)。Ang-2在GnRHa治疗后的表达情况:OEMs者在位内膜中的表达(60.87%)虽然低于未治疗组(80.00%),但差异无统计学意义(P>0.05),但仍明显高于对照组(21.48%)(P<0.05),异位内膜组织中的表达治疗组(30.43%)显著低于未治疗组(52.00%)(P<0.05),在位内膜中的表达仍显著高于异位内膜(P<0.05)。结论 Ang-2在子宫内膜异位症发生发展中起到重要的作用,GnRHa对异位内膜中的Ang-2表达有抑制作用。
Objective To investigate the role of angiopoietin-2 (Ang-2) in the development and progression of endometriosis (EMs) and the role of gonadotropin-releasing hormone analogue (GnRHa) Effect of Ang-2 expression in ectopic endometrium. Methods Twenty-five patients with ovarian endometriosis (OEMs) were selected as untreated group. 23 patients with OEMs received 3 courses of GnRHa preoperatively and 28 women with non-endometrial disease as control group. The endometriums were harvested and the expression of Ang-2 in eutopic endometrium and normal endometrium was detected by immunohistochemistry in ectopic and non-treated OEMs. Results Ang-2 protein mainly located in the cytoplasm of endometrial glandular epithelial cells. In the untreated group, the positive expression rate of Ang-2 in eutopic endometrium of OEMs group was 80.00%, which was significantly higher than that of ectopic endometrium (52.00%) and control group (21.48%) (P <0.05) The positive expression rate in endometriosis group was 52.00%, which was significantly higher than that in control group (21.48%) (P <0.05). Ang-2 expression after GnRHa treatment: The expression of endometriosis in OEMs (60.87%) was lower than that in untreated group (80.00%), but the difference was not statistically significant (P> 0.05) (21.48%) (P <0.05). The expression of ectopic endometrial tissue in the treatment group (30.43%) was significantly lower than that in the untreated group (52.00%) (P <0.05) The expression was still significantly higher than the ectopic endometrium (P <0.05). Conclusion Ang-2 plays an important role in the development of endometriosis. GnRHa can inhibit the expression of Ang-2 in the ectopic endometrium.