摘要
目的探讨感染引发胎膜早破的可能机制。方法取20例正常择期剖宫产孕妇(无妊娠合并症、并发症,也无临产征兆)的胎膜在体外进行孵育,共分成4组:0h组(取下后未经孵育的胎膜)、24h组、48h组、72hLPS组。首先评价体外孵育胎膜的存活力,然后应用免疫组织化学方法分别测定4组胎膜的基质金属蛋白酶-9(MMP-9)及金属蛋白酶组织抑制因子-1(TIMP-1)在蛋白水平的表达变化,最后分析72hLPS组MMP-9/TIMP-1比值的变化。结果体外孵育胎膜的总存活力达到(83±1.9)%,免疫组化染色结果可见0h组及48h组的MMP-9表达微弱,24h组的表达较前2组增强,72h组的表达最强,各组TIMP-1的表达无明显区别,72h组MMP-9/TIMP-1比值上升。结论MMP-9/TIMP-1比值升高可能是感染引发胎膜早破的机制之一。
Objective To explore the possible mechanism of premature rupture of membranes （PROM） caused by infection. Methods Amniochorionie membranes were collected from 20 pregnant women undergoing elective cesarean section at term, without evidence of active labor or complications of pregnancy. The amniochorionic membranes were then cultured and divided：into 4 groups： 0 hour group, 24 hour group, 48 hour group and 72 hour LPS （liptgpolysaccharide） group （In some of the 48 h culures, LPS was added before the culture was continued to constitute the 72 hour LPS group）. The viability of the cultured membranes was determined in terms of LDH; the expressions of matrix metalloproteinnase - 9 （ MMP - 9 ） and tissue inhibitor of metalloproteinase - 1 （ TIMP - 1 ） , by immunohistochemistry （ HIC ）. Results The viability of cultured amniochorionic membranes reached （83 ± 1.9） %. HIC showed that the expression of MMP -9 was not altered in the 0 hour group and 48 hour group, slightly elevated in the 24 hour group, markedly elevated in the 72 hour LPS group. No changes were noticed in the expression of TIMP - 1 in any of the 4 groups. The ratio of MMP - 9/TIMP - 1 in the 72 hour LPS group was elevated evidently （ P 〈 0.05 ） . Conclusion Elevation of the MMP -9/TIMP - 1 ratio may be one of the mechanisms of PROM related to infection.
出处
《徐州医学院学报》
CAS
2008年第1期46-49,共4页
Acta Academiae Medicinae Xuzhou
关键词
基质金属蛋白酶
胎膜早破
感染
细菌内毒素脂多糖
免疫组织化学
matrix metalloproteinase
premature rupture of membranes （PROM）
infection
liptopolysaccharide （LPS）
immunohistochemistry （ HIC ）
