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目的探讨浸润相关蛋白MT1-MMP与RECK在子宫腺肌病(AM)中的表达及二者与血管生成的联系,进一步分析AM的可能发病机制。方法 2012年2月-2013年2月在泸州医学院附属医院收集并筛选出78例AM患者的子宫异位内膜(异位组)和非异位区宫腔面内膜(在位组)及69例子宫肌瘤患者的宫腔面非肌瘤区内膜(对照组),免疫组化检测3组内膜MT1-MMP与RECK的表达,CD34标记后计数微血管密度MVD,分析3者相关性。结果 3组中MT1-MMP的表达及MVD值均呈异位组>在位组>对照组的趋势,组间比较,差异有统计学意义(P<0.05)。在位组RECK的表达高于异位组,差异有统计学意义(P<0.05),对照组虽高于在位组,但差异无统计学意义(P>0.05)。3组MT1-MMP与RECK的表达均呈负相关性(P>0.05);在异位组和在位组中,MT1-MMP与MVD均呈正相关(P<0.05),RECK与MVD均呈负相关(P<0.05),在对照组中,MT1-MMP、RECK与MVD均无相关性(P>0.05)。结论 MT1-MMP与RECK的异常表达可能是AM发病中促进内膜异位、浸润生长并参与异位区血管形成的重要原因。
Objective To investigate the expression of infiltration-related proteins MT1-MMP and RECK in adenomyosis (AM) and the relationship between them and angiogenesis and further analyze the possible pathogenesis of AM. Methods From February 2012 to February 2013, 78 cases of uterine ectopic endometrium (ectopic group) and non-ectopic uterine cavity endometrium (eutopic group) were collected and screened in Luzhou Medical College Affiliated Hospital. And 69 cases of uterine fibroids in uterine fibroids area (control group). Immunohistochemistry was used to detect the expression of MT1-MMP and RECK in the intima of the three groups and the MVD of the microvessel density Sex. Results The MT1-MMP expression and MVD in 3 groups showed the trend of ectopic group> eutopic group> control group. There was significant difference between groups (P <0.05). The expression of RECK in the eutopic group was significantly higher than that in the ectopic group (P <0.05), while the control group was higher than the eutopic group (P> 0.05). There was a negative correlation between the expression of MT1-MMP and RECK in the three groups (P> 0.05). MT1-MMP was positively correlated with MVD in ectopic and eutopic groups (P <0.05), while both RECK and MVD were negative (P <0.05). There was no correlation between MT1-MMP, RECK and MVD in the control group (P> 0.05). Conclusion The abnormal expression of MT1-MMP and RECK may play an important role in promoting the development of endometriosis, infiltration and angiogenesis in the pathogenesis of AM.