摘要
目的探讨米非司酮治疗子宫腺肌症的机制是否与其纠正了基质金属蛋白酶-9(MMP-9)和组织金属蛋白酶抑制物-1(TIMP-1)在异位内膜的表达失衡有关。方法35例行全子宫切除术的子宫腺肌症患者分为米非司酮治疗组(n=19)和对照组(n=16)。子宫内膜作为在位内膜标本,腺肌瘤作为异位内膜标本,采用免疫组化法测定并比较在位和异位内膜中MMP-9和TIMP-1水平。结果米非司酮治疗组异位内膜组织中,MMP-9在腺上皮细胞内的表达显著低于对照组(P<0.05),TIMP-1的表达显著高于对照组(P<0.05),MMP-9/TIMP-1的比值显著低于对照组(P<0.05)。结论子宫腺肌症患者经过米非司酮治疗后,异位内膜中MMP-9表达下降,TIMP-1表达上升;米非司酮通过下调MMP-9/TIMP-1的比值来控制异位内膜组织的种植侵袭。
To study whether the mechanism of mifepristone in treating adenomyosis is suppressing matrix metalloproteinase-9 and tissue inhibitors of metalloproteinase-1 （ MMP-9/TIMP-1 ）. Methods Thirty-five patients in the mifepristone treated group （ 19 cases of adenomyosis） and the control group （16 cases of adenomyosis, non-drug treated） underwent hysterectomy. Endometrium was looked as eutopic endometrium and adenomyosis as ectopic endometrium. Expression of MMP-9 and TIMP-1 in eutopic and ectopic endometfium were measured by immunohistochemical techniques. Results The ectopic endometrium of the mifepristone treated group expressed lower level of MMP-9, higher level of TIMP-1 and lower ratio of MMP-9/TIMP-1 than the ectopic endometrium of the control group （P 〈 0.05）. Conclusion In patients with adenomyosis treated with mifepristone, MMP-9 expression decreases and TIMP-1 expression increases. Mifepristone could reduce the ratio of MMP-9/TIMP-1 to prevent the evolution of adenomyosis.
出处
《上海交通大学学报（医学版）》
CAS
CSCD
北大核心
2007年第8期981-983,共3页
Journal of Shanghai Jiao tong University:Medical Science
基金
上海市科委基金(C0303)~~
