黏附分子VCAM-1和ICAM-1在子宫内膜异位症中的表达及意义
发布时间：2018-12-18 07:07
【摘要】：目的:探讨血管细胞黏附分子(VCAM-1)和细胞间黏附分子(ICAM-1)在子宫内膜异位症(EMT)发病中的作用及意义。方法:采用荧光定量聚合酶链反应技术(Real-Time PCR)和免疫印迹法(Western-Blot)分别检测EMT(15例)患者异位内膜、在位内膜和对照组(15例)子宫内膜中VCAM-1、ICAM-1mRNA及蛋白的表达情况。采用双抗夹心酶联免疫吸附实验(ELISA)检测EMT组(44例)与对照组(28例)中可溶性VCAM-1(s VCAM-1)和可溶性ICAM-1(s ICAM-1)的水平,并对VCAM-1、ICAM-1在不同组中的mRNA、蛋白及血清中的表达行相关性分析。结果:1EMT异位内膜组VCAM-1、ICAM-1mRNA的表达均明显高于在位内膜组及对照组(P0.01);在位内膜组VCAM-1、ICAM-1mRNA的表达与对照组差异无统计学意义(P0.05)。2EMT异位内膜组VCAM-1、ICAM-1蛋白的表达明显高于在位内膜组及对照组(P0.01),在位内膜组VCAM-1蛋白表达高于对照组(P0.01);EMT在位内膜组ICAM-1蛋白的表达与对照组比较差异无统计学意义(P0.05)。3EMT患者血清中s VCAM-1和s ICAM-1水平均明显高于对照组(P0.01),Ⅲ、Ⅳ期患者血清中s ICAM-1水平较Ⅰ、Ⅱ期患者明显升高(P0.01)。4EMT异位内膜组组织中VCAM-1与ICAM-1在mRNA、蛋白表达及血清中的水平均无相关性(P0.05)。结论:异位内膜的VCAM-1和ICAM-1的表达异常可能在EMT的发生发展中具有重要作用,但ICAM-1与VCAM-1在EMT中可能具有各自的信号通路及蛋白表达的途径。
[Abstract]:Objective: to investigate the role and significance of vascular cell adhesion molecules (VCAM-1) and intercellular adhesion molecules (ICAM-1) in the pathogenesis of (EMT) in endometriosis. Methods: using fluorescent quantitative polymerase chain reaction (Real-Time PCR) and Western blotting (Western-Blot) to detect VCAM-1, in ectopic endometrium, eutopic endometrium and control group (15 cases) of EMT patients, respectively. Expression of ICAM-1mRNA and protein. The levels of soluble VCAM-1 (s VCAM-1) and soluble ICAM-1 (s ICAM-1) in EMT group (44 cases) and control group (28 cases) were detected by double antibody sandwich enzyme linked immunosorbent assay (ELISA). The correlation between mRNA, protein and serum expression of ICAM-1 in different groups was analyzed. Results: the expression of VCAM-1,ICAM-1mRNA in ectopic endometrium of 1EMT was significantly higher than that in eutopic endometrium and control group (P0.01). There was no significant difference in VCAM-1,ICAM-1mRNA expression between eutopic endometrium group and control group (P0.05). The expression of VCAM-1,ICAM-1 protein in 2EMT ectopic endometrium group was significantly higher than that in eutopic endometrium group and control group (P0.01). The expression of VCAM-1 protein in eutopic endometrium group was higher than that in control group (P0.01). The expression of ICAM-1 protein in the eutopic endometrium of EMT was not significantly different from that in the control group (P0.05). The levels of s VCAM-1 and s ICAM-1 in the patients with 3EMT were significantly higher than those in the controls (P0.01, 鈪，
本文编号：2385535
[Abstract]:Objective: to investigate the role and significance of vascular cell adhesion molecules (VCAM-1) and intercellular adhesion molecules (ICAM-1) in the pathogenesis of (EMT) in endometriosis. Methods: using fluorescent quantitative polymerase chain reaction (Real-Time PCR) and Western blotting (Western-Blot) to detect VCAM-1, in ectopic endometrium, eutopic endometrium and control group (15 cases) of EMT patients, respectively. Expression of ICAM-1mRNA and protein. The levels of soluble VCAM-1 (s VCAM-1) and soluble ICAM-1 (s ICAM-1) in EMT group (44 cases) and control group (28 cases) were detected by double antibody sandwich enzyme linked immunosorbent assay (ELISA). The correlation between mRNA, protein and serum expression of ICAM-1 in different groups was analyzed. Results: the expression of VCAM-1,ICAM-1mRNA in ectopic endometrium of 1EMT was significantly higher than that in eutopic endometrium and control group (P0.01). There was no significant difference in VCAM-1,ICAM-1mRNA expression between eutopic endometrium group and control group (P0.05). The expression of VCAM-1,ICAM-1 protein in 2EMT ectopic endometrium group was significantly higher than that in eutopic endometrium group and control group (P0.01). The expression of VCAM-1 protein in eutopic endometrium group was higher than that in control group (P0.01). The expression of ICAM-1 protein in the eutopic endometrium of EMT was not significantly different from that in the control group (P0.05). The levels of s VCAM-1 and s ICAM-1 in the patients with 3EMT were significantly higher than those in the controls (P0.01, 鈪，
本文编号：2385535
本文链接：https://www.wllwen.com/yixuelunwen/fuchankeerkelunwen/2385535.html
最近更新
教材专著
