MMP-9、TIMP-1在子宫内膜异位症患者子宫内膜中的表达及意义

Expression and significance of MMP-9 and TIMP-1 in endometriosis

目的观察基质金属蛋白酶-9(MM P-9)和基质金属蛋白酶组织抑制剂-1(T IM P-1)在子宫内膜异位症(EM s)患者子宫内膜中的表达,并探讨其在EM s发病机制中的作用。方法利用免疫组化法检测MM P-9和T IM P-1在35例EM s患者(观察组,其中未孕16例、已孕19例)异位内膜及在位内膜组织和35例正常人(对照组)子宫内膜中的表达。结果①MM P-9在观察组异位内膜中的表达高于在位内膜和对照组(P均<0.05),在位内膜中的表达高于对照组(P均<0.05);②T IM P-1、MM P-9/T IM P-1在观察组异位内膜中的表达低于在位内膜和对照组(P均<0.05);观察组未孕与已孕患者MM P-9和T IM P-1表达以及MM P-9/T IM P-1均无统计学差异(P均>0.05)。结论MM P-9高表达以及MM P-9/T IM P-1的比例失调,使子宫内膜更具侵袭性,在EM s的发生、发展中起重要作用。

[Objective] To observe the expression of matrix metalloproteinases-9 （MMP-9） and tissue inhibitors of matrix metalloproteinases-1 （TIMP-1） in endometriosis, and study the possible role of MMP-9 and TIMP-1 in the pathogenesis of endometriosis. Methods： Expression of MMP-9 and TIMP-1 in 35 normal endometrium as well as 35 ectopic endometrium and eutopic endometrium in endometriosis （16 nonfertile patients and 19 patients who had been pregnant） were detected by immunohistochemistry and the results were analyzed with SPSS11. 0 statistical solfware. [Results] ①The expression level of MMP-9 in the ectopic endometriotic tissues was significantly higher than those in the eutopic endometrium and normal endometrium （P both 0. 05）. ②Theexpression level of TIMP-1 in the ectopic endometriotic tissues was significantly lower than those in the eutopic endometrium and normal endometrium （P〈0. 05）. ③The gray scale ratio of MMP-9/TIMP-1 in the ectopic endometriotic tissues was significantly lower than those in the eutopic endometrium and normal endometrium （P〈0. 05）. ④In the eetopic and eutopic endometriotic tissues and normal endometrium, there had no statistical difference between the nonfertile patients and the patients who had been pregnant in the expression level of MMP-9 and TIMP-1 and the gray scale ratio of MMP-9/TIMP-1 （P〉0. 05）. [Conclusion]： The excessive expression of MMP-9 in ectopic endometriotic tissues and the disproportion of MMP-9/TIMP-1 makes the ectopic endometriotic tissues to have more invasive ability, which contributes to the pathogenesis of endometriosis.