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CD44v6、Smad7在子宫内膜异位症中表达的研究
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摘要
目的:检测CD44v6和Smad7在子宫内膜异位症中的表达及其相关性,探讨CD44v6和Smad7在子宫内膜异位症发病中的作用。
     方法:采用免疫组织化学法(IHC)检测子宫内膜异位症异位内膜(30例)、在位内膜(25例)及正常子宫内膜(30例)中CD44v6和Smad7的表达情况。
     结果:CD44v6在子宫内膜异位症异位内膜组的表达以强阳性为主,而在在位内膜组和对照组内膜组织中的表达以阴性和弱阳性为主。异位内膜组CD44v6的免疫活性高于在位内膜组和对照组,差异均有统计学意义(P=0.001<0005,P=0.001<0.05);对照组CD44v6的免疫活性高于在位内膜组,差异有统计学意义(P=0.028<0.05);在位内膜组、对照组中分泌期内膜组织中CD44v6的免疫活性分别高于其同组增生期,差异有统计学意义(P=0.035<0.05,P=0.01<0.05)。
     Smad7在子宫内膜异位症异位内膜组、在位内膜组的表达以弱阳性和阴性为主,而在对照组内膜组织中的表达以强阳性为主。异位内膜组、在位内膜组Smad7的免疫活性低于对照组,差异均有统计学意义(P=0.046<0.05,P=0.044<0.05);异位内膜组与在位内膜组Smad7的免疫活性比较,差异无统计学意义(P=0.899>0.05);在位内膜组、对照组分泌期内膜组织中Smad7的免疫活性与其同组增生期相比,差异无统计学意义(P=0.521>0.05,P=0.499>0.05)。
     CD44v6及Smad7在各组子宫内膜组织的表达水平呈不相关关系(P>0.05)。
     结论:1.CD44v6在子宫内膜异位症表达增强,Smad7在子宫内膜异位症异表达减弱,提示CD44v6、Smad7可能参与内异症发病过程。
     2.CD44v6及Smad7在各组子宫内膜组织中的表达水平呈不相关关系,提示两者可能通过不同的途径调节内异症的发病过程。
Objective: To investigate the expression and the relativity of CD44v6 and Smad7 in endometriosis for exploring the role of CD44v6 and Smad7 in the pathogenesis of endometriosis.
     Methods: Immunohistochemistry was used to detect the expression of CD44v6 and Smad7 in the ectopic endometrium of 30 cases (ectopic endometrium group) , in the eutopic endometrium of 25 cases (eutopic endometrium group) with endometriosis and in the normal endometrium of 30 cases without endometriosis (control group).
     Results: The CD44v6 in ectopic endometrium group with strong positive expression mainly , in the eutopic endometrium group and the control group with main negative and weakly positive expression . The CD44v6 immunoreactivity of ectopic endometrium group was higher than that of eutopic endometrium group and the control group , the differences were statistically significant (P=0.001<0.05, P=0.001<0.05 ); increased expression of CD44v6 immunoreactivity was detected in control group compared with eutopic endometrium group , the difference was ststistically significant (P=0.028 <0.05 ) ; we also found CD44v6 in eutopic endometrium group and the control group of the secretory phase endometrium tissues , respectively , higher than the proliferative phase with the group , the differences were statistically significant (P=0.035<0.05, P=0.01<0.05).
     The Smad7 in ectopic endometrium group and eutopic endometrium group with negative and weakly positive expression mainly , in the control group with strong positive expression. The Smad7 immunoreactivity of ectopic endometrium and eutopic endometrium group were lower than that of the control group , the differences were statistically significant (P=0.046<0.05 , P=0.044<0.05) ; the Smad7 immunoreactivity of ectopic endometrium compared with the eutopic group, the difference was not statistically significant (P=0.899 >0.05) ; the expression of the Smad7 in the proliferative phase endometrium compared with secretory of eutopic endometrium group and control group, the differences were not statistically significant (P=0.521 >0.05, P=0.499>0.05) .
     The expression of CD44v6 had no corralation with that of Smad7 in each group endometrium (P>0.05).
     Conclusion:
     1. The up regulation of CD44v6 and the low regulation of Smad7 in endometriosis suggest that CD44v6 and Smad7 may play a role in the pathogenesis of endometriosis.
     2. The expression of CD44v6 had no corralation with that of Smad7 in each group endometrium , suggest that the pathogenesis of endometriosis may be regulated by them in different ways.
引文
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