研究基质金属蛋白酶-7(MMP-7)、基质金属蛋白酶抑制因子-1(TIMP-1)在子宫腺肌病中的表达，探讨二者之间的相关性及其在子宫腺肌病发病机制中的作用。

采用免疫组化链霉菌抗生物素蛋白-过氧化物酶连接(SP)法，检测78例子宫腺肌病患者的原位内膜、异位内膜及80例正常子宫内膜中MMP-7和TIMP-1表达情况。

①MMP-7在子宫腺肌病原位内膜、异位内膜中的表达显著高于正常子宫内膜，差异有显著意义(P<0. 05);②TIMP-1在正常子宫内膜的表达高于腺肌病的原位内膜、异位内膜，差异有显著意义(P<0. 05)。③在正常子宫内膜组织中MMP-7与TIMP-1之间具有负相关关系，在腺肌病的原位内膜、异位内膜中二者不具有相关性。

MMP-7表达增强和MMP-7/TIMP-1的比例失调，是子宫腺肌病的原位内膜及异位内膜细胞具有侵袭能力的原因之一，从而为治疗本病提供了循证医学依据。

To observe the expression of matrix metalloproteinase-7(MMP-7)and tissue inhibitors of matrix metalloproteinase-1(TIMP-1)in adenomyosis. To explore the correlation between the expression of MMP-7 and TIMP-1 in adenomyosis, and to study the possible role of MMP-7 and TIMP-1 in the pathogenesis of adenomyosis.

The expression of MMP-7 and TIMP-1 in 78 ectopic and eutopic endometrium in adenomyosis were detected by immunohistochemical methods in comparison with 80 normal endometrium.

① the expression levels of MMP-7 in ectopic and eutopic of adenomyosis tissues were significantly higher than those in the normal endometrium(P<0. 05). ②The expression levels of TIMP-1 on ectopic and eutopic endometrium of adenomyosis were controlled with normal endometrium, P<0. 05, having statistical significance.③ there was significantly negative correlation between expression of MMP-7 and TIMP-1 in normal endometrium. but there was no correlation in ectopic and eutopic endometrium of adenomyosis.

The high expression of MMP-7 and the lopside development on MMP-7/TIMP-1 ratio may participate in the process of invasion and tissue modeling that is hypothesized to occur in the pathogenesis of adenomyosis.