关键词: 子宫腺肌病, 环氧合酶2, β-连环蛋白, 痛经, 视觉模拟评分

Abstract:

Objective To discuss the expression levels of cyclooxygenase-2 （COX-2） and β-catenin in the in situ endometrium tissue， lesion tissue， and serum of the adenomyosis （AM） patients，and to clarify their relationships with dysmenorrhea. Methods A total of 90 cases of confirmed AM patients with dysmenorrhea who underwent abdominal hysterectomy were selected as AM group， and 30 cases of patients with uterine myomas （UM） without dysmenorrhea were selected as UM group. The degree of dysmenorrhea of the AM patients was assessed by using the visual analogue scale （VAS）， and 90 cases of AM patients were divided into mild dysmenorrhea group， moderate dysmenorrhea group， and severe dysmenorrhea group （n=30）. Immunohistochemistry （IHC） was used to detect the expression levels of COX-2 and β-catenin proteins in endometrium tissue of the patients in two groups； enzyme-linked immunosorbent assay （ELISA） method was used to detect the levels of COX-2 and β-catenin in serum of the patients in two groups；the association between the expression levels of COX-2 and β-catenin in endometrium tissue of the patients in two groups and degree of dysmenorrhea of the patients was analyzed by Spearman correlation analysis. Results The COX-2 protein expression was mainly located in the cytoplasm of endometrium tissue， while β-catenin protein was mainly expressed in the cell membrane or cytoplasm of endometrium tissue. Compared with UM group， the expression levels of COX-2 protein in in situ endometrium tissue and lesion tissue of the patients in AM group were increased（P<0.05），and the expression level of β-catenin protein was decreased（P<0.05）. Compared with in situ endometrium tissue of the patients in AM group， the expression level of COX-2 protein in lesion endometrium tissue of the patients in AM group was increased（P<0.05）.The expression level of COX-2 protein in the lesion tissue of the AM patients with moderate dysmenorrhea and the expression level of COX-2 protein in in situ endometrium and lesion tissues of the AM patients in severe dysmenorrhea group were significantly higher than those in mild dysmenorrhea group（P<0.05）； the expression level of COX-2 protein in in situ endometrium and lesion tissues of the AM patients in severe dysmenorrhea group were significantly higher than those in moderate dysmenorrhea group（P<0.05）.There were no significant differences in the expression levels of β-catenin protein in in situ endometrium tissue and lesion tissue of the AM patients between different degrees of dysmenorrhea groups （P>0.05）. Compared with UM group，the serum level of COX-2 of the patients in AM group was significantly increased （P<0.05），and the serum levels of β-catenin of the patients in AM group was decreased （P<0.05）.Compared with mild dysmenorrhea group，the serum COX-2 levels of the patients in moderate and severe dysmenorrhea groups were increased（P<0.05）. There were no significant differences in serum β-catenin level of the patients between different degrees of dysmenorrhea groups （P>0.05）.The expression level of COX-2 protein in lesion tissue of the AM patients was negatively correlated with the expression level of β-catenin protein （r=－0.364， P<0.05）； in in situ endometrium and lesion tissues of the AM patients， the expression level of COX-2 protein was positively correlated with the degree of dysmenorrhea （r=0.511，P<0.05； r=0.696， P<0.05）， suggesting that the expression level of COX-2 protein was positively correlated with the degree of dysmenorrhea and there was no correlation between the expression level of β-catenin protein and the degree of dysmenorrhea （P>0.05）. The correlation between the serum levels of COX-2 and β-catenin of the patients were negative （r=－0.534， P<0.05）， and the COX-2 level of the patients was positively correlated with the degree of dysmenorrhea （r=0.613， P<0.05）. Conclusion The increasing of expression level of COX-2 and decreasing of expression level of β-catenin and their correlation both induce AM development and endometriotic invasion， and high expression of COX-2 may promote the dysmenorrhea， which may serve as a potential molecular target for the treatment of AM and associated dysmenorrhea.

Key words: Adenomyosis, Cyclooxygenase-2, β-catenin, Dysmenorrhea, Visual analogue scale