卵巢子宫内膜异位症患者异位及在位内膜组织中COX-2的表达及意义

目的:检测卵巢子宫内膜异位症患者异位内膜组织和在位内膜组织及正常人子宫内膜组织中COX-2的表达,以探讨环氧合酶COX-2在卵巢子宫内膜异位症的在位内膜和异位内膜中的表达及COX-2在子宫内膜异位症发生、发展中的作用。方法:通过免疫组化方法检测45例正常人子宫内膜及45例卵巢子宫内膜异位症患者在位及异位子宫内膜中COX-2的表达。结果;正常人表面上皮细胞和腺上皮细胞COX-2的表达在月经周期中明显变化。在增生早期最低,然后逐步增高。在整个分泌期维持高水平直至月经期达高峰。在子宫内膜异位症患者中,尽管其随月经周期变化,但是和正常人同期相比表达增高。在子宫内膜异位症患者中,卵巢巧克力囊肿异位内膜中腺细胞中观察到明显的COX-2高表达,比正常人分泌期和月经期高。正常人子宫内膜、子宫内膜异位症患者在位子宫内膜、子宫内膜异位症患者异位子宫内膜3组的COX-2表达存在统计学差异(P<0.01)。结论:COX-2在正常人子宫内膜组织中有表达且在月经周期中发生一定变化;COX-2在卵巢子宫内膜异位症患者异位内膜组织中过度表达:COX-2与卵巢子宫内膜异位症发生、发展关系密切。

The expression and its meaning of Cyclooxygenase-2 (COX-2 ) in eutopic and ectopic endometria in endometriosis and in eutopic endometria

Objective:To explore the expression of Cyclooxygenase-2(COX-2 ) in eutopic and ectopic endometria in endometriosis and in eutopic endometria in control women, and the effect of the occurernce and progress ofendometriosis.Methods:The subjects were examined immunohistochemically.Results:The expression of COX-2 in surface and glandular epithelia of the control gro'dp varied markedly during the menstrual cycle.It was lowest in the early proliferative phase and gradually increased thereafter. It remained high throughout the secretory phase. However, in patients with endometriosis, expression of COX-2 in glandular epithelium was higher than that in the control group, though it varied throughout the menstrual cycle.Overexpression COX-2 was observed in glandular cells from ectopic endometrial tissue of ovarian chocolate cyst walls in all cases regardless of the menstrual phase(P<0.01) among eutopic endometrium the control group, eutopic endometrium in the endometriosis group and ectopic endometrium in ovarian endometriosis by the Kruskai-Wallis test.Conclusion:The expression of COX-2 in surface and glandular epithelia of the control group varied markedly during the menstrual cycle. Overexpression COX-2 was observed in glandular cells from ectopic endometrial tissue of ovarian chocolate cyst walls of endometriosis.There is some close relationship between the over expression of COX-2 and the occurrence and progression of ovarian endometriosis.