Abstract
Adenomyosis is a common gynecologic disease that severe impact on women. Previous studies have found that Bcl-2 abnormally expressed in adenomyosis. However, the exact mechanisms of Bcl-2 in the pathogenesis of adenomyosis are unclear. In this study, we are to explore the effect of Bcl-2 on proliferation, migration, and apoptosis of endometrial stromal cells. The expression of Bcl-2 were evaluated by Western blot and RT-qPCR. We used RNA interference to silence Bcl-2 gene of endometrial stromal cells, and then Cell Counting Kit(CCK-8), cell scratch repair test, and Annexin V-APC/propidium iodide (PI) staining were performed to detect the cell viability, migration ability and apoptotic rate. The results of the present study revealed that the expression of Bcl-2 was evidently higher than that in control group. After silencing the Bcl-2 gene, the cytoactive and migration ability of endometrial stromal cells of adenomyosis decreased, and the apoptotic rate increased. In conclusion, Bcl-2 is overexpressed in adenomyosis and participate in the pathogenesis of adenomyosis. Bcl-2 may be a potential novel target for adenomyosis treatment.
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