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肿瘤坏死因子α及孕酮对异位子宫内膜间质细胞分泌基质金属蛋白酶-3的调节
引用本文:翦薇,何福仙.肿瘤坏死因子α及孕酮对异位子宫内膜间质细胞分泌基质金属蛋白酶-3的调节[J].现代妇产科进展,2004,13(6):410-412.
作者姓名:翦薇  何福仙
作者单位:华中科技大学同济医学院附属同济医院妇产科,武汉,430030
摘    要:目的 :探讨细胞因子、性激素与基质金属蛋白酶 (MMPs)在子宫内膜异位症(EMs)发病机制中的作用及相关性。方法 :以EMs患者 15例作研究组 ,分别取其在位与异位内膜 ,以非EMs患者 10例的正常内膜为对照组。原代培养子宫内膜间质细胞 ,在研究组和对照组内分别设置空白对照组、孕酮组与肿瘤坏死因子 α(TNF α)组。孕酮组分别加入孕酮 10 - 7mol/L、10 - 5mol/L ,各孵育 2 4h ;TNF α组中加入TNF α 10 0ng/L ,分别孵育2 4h、4 8h。ELISA法检测MMP 3含量。结果 :空白对照组MMP 3含量 ,异位组显著高于在位内膜组与对照组 (P <0 .0 1)。加入孕酮后各组MMP 3含量均呈下降趋势 ,异位组下降程度更为显著 (P <0 .0 1) ,高浓度孕酮具有更强的抑制作用 (P <0 .0 5 )。TNF α干扰后 ,各组MMP 3含量均升高 (P <0 .0 1) ,以异位组显著 (P <0 .0 1) ,不同作用时间对MMP 3含量的影响各组间无显著差异 (P >0 .0 5 )。结论 :EMs患者子宫内膜间质细胞分泌MMP 3较正常人高 ,异位病灶分泌能力更强。TNF α和孕酮对MMP 3的分泌分别有升调与降调的作用 ,二者可能通过此途径参与了EMs的发生发展过程。

关 键 词:子宫内膜异位症  肿瘤坏死因子α  孕酮  基质金属蛋白酶
文章编号:1004-7379(2004)06-0410-03
修稿时间:2004年5月10日

Adjustment of matrix metalloproteinase-3 in ectopic endometrial stromal cells by TNF-α and progestrone
Jian Wei,He Fuxian.Adjustment of matrix metalloproteinase-3 in ectopic endometrial stromal cells by TNF-α and progestrone[J].Current Advances In Obstetrics and Gynecology,2004,13(6):410-412.
Authors:Jian Wei  He Fuxian
Institution:Jian Wei,He Fuxian.Department of Obstetrics and Gynecology,Tongji Medical College,Huazhong University of Science and Techno logy,Wuhan 430030
Abstract:Objective:To evaluate the roles of cytokine,sex hormone s and matrix metalloproteinase-3(MMP-3) in ectopic endometial stromal cells by T NF-α and progesterone.Method:Concentrations of MMP-3 were d etermined by ELISA. Fifteen patients with endometriosis were included as study g roup and ten patients without endometriosis as contr ol group.Results:Levels of MMP-3 in endometrial stromal cells were significantly different(P<0.01),the ectopic group was sig nificantly higher than the eutopic group and the control g roup (P<0.01). Secretion of MMP-3 in each group decreased i n culture with progesterone;there was significant difference between the study group and the control group (P<0.01).Level of decrease in ectopic group was significantly higher than that of other two groups (P<0.01). Secretion of MMP-3 in each group increased in culture with TNF- α. Level of increase in the ectopic group was higher than that in the eutopic g roup and the control group (P<0.01).Conclusion:TNF-α ma y play role in pathogenesis of endometriosis by increasing the secreation of MMP -3 in endome trial stromal cells. Progesterone can decrease the secretion of MMP-3 and it ma y restrain the development of endometriosis.
Keywords:Endometriosis  Tumor necrosis factor-alpha  Progesterone  Matrix metalloproteinases
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