The journal of obstetrics and gynaecology research · 2020
Immunohistochemical expression of estrogen receptor α, Bcl-2 and NF-κB P65 in the polyps of patients with and without endometriosis.
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Jiang Rufang, Yang Yihua, Huang Qiuyan, Jin Yufu, Feng Yu, Huang Xinyue, Qin Aiping, Liu Bo
Аннотация
AIM: To compare the expression of estrogen receptor α (ERα), Bcl-2 and NF-κB P65 in endometrial polyps from patients with and without endometriosis.
METHODS: Immunohistochemistry was used to characterize the expression of ERα, Bcl-2 and NF-κB P65 in proliferative phase endometrial polyps from patients with and without endometriosis. H-Scores indicating the staining intensity for ERα, Bcl-2 and NF-κB P65 in the glandular epithelium and stroma were measured separately. Apoptotic cells were detected with the use of the dUTP nick-end labeling (TUNEL) assay.
RESULTS: Bcl-2 was expressed in the cytoplasm of glandular epithelial cells, whereas ERα was expressed in the nuclei of both glandular epithelial and stromal cells. NF-κB P65 was observed in the cytoplasm of both glandular epithelial and stromal cells. The H-scores for Bcl-2 in the endometrial glands significantly higher in the endometriosis polyp group than in the non-endometriosis polyp group. The H-scores for ERα in both stromal and glandular epithelial cells were significantly higher in the endometriosis polyp group than in the non-endometriosis polyp group. The H-scores for Bcl-2 and ERα were positively correlated in all of the women examined. Apoptotic cells in the endometriosis polyp group were significantly less than that of the non-endometriosis polyp group.
CONCLUSION: There expression levels of Bcl-2 and ERα, both of which were significantly increased in the polyps of endometriosis patients compared to those of patients without endometriosis, were positively correlated. These results suggested that imbalanced apoptosis secondary to abnormally high ERα expression was responsible for the high prevalence of polyps in endometriosis patients.
METHODS: Immunohistochemistry was used to characterize the expression of ERα, Bcl-2 and NF-κB P65 in proliferative phase endometrial polyps from patients with and without endometriosis. H-Scores indicating the staining intensity for ERα, Bcl-2 and NF-κB P65 in the glandular epithelium and stroma were measured separately. Apoptotic cells were detected with the use of the dUTP nick-end labeling (TUNEL) assay.
RESULTS: Bcl-2 was expressed in the cytoplasm of glandular epithelial cells, whereas ERα was expressed in the nuclei of both glandular epithelial and stromal cells. NF-κB P65 was observed in the cytoplasm of both glandular epithelial and stromal cells. The H-scores for Bcl-2 in the endometrial glands significantly higher in the endometriosis polyp group than in the non-endometriosis polyp group. The H-scores for ERα in both stromal and glandular epithelial cells were significantly higher in the endometriosis polyp group than in the non-endometriosis polyp group. The H-scores for Bcl-2 and ERα were positively correlated in all of the women examined. Apoptotic cells in the endometriosis polyp group were significantly less than that of the non-endometriosis polyp group.
CONCLUSION: There expression levels of Bcl-2 and ERα, both of which were significantly increased in the polyps of endometriosis patients compared to those of patients without endometriosis, were positively correlated. These results suggested that imbalanced apoptosis secondary to abnormally high ERα expression was responsible for the high prevalence of polyps in endometriosis patients.