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Updated: Aug 20, 2025
Isolation of Human Endometrial Stromal Cells for In Vitro Decidualization
Published on: September 1, 2018
Dienogest May Reduce Estradiol- and Inflammatory Cytokine-Induced Cell Viability and Proliferation and Inhibit the
Hyun Jin Kim1, Sung Hoon Kim1, Young Sang Oh1
1Department of Obstetrics and Gynecology, University of Ulsan College of Medicine, Asan Medical Center, Seoul 05505, Republic of Korea.
Abstract:
Dienogest (DNG) is a therapeutic medication used in endometriosis treatment. Limited data are available regarding its mechanism of action on endometrial cells. Using in vivo and in vitro models, we investigated whether DNG treatment causes significant biological changes in human endometrial stromal cells (ESCs). The markers related to the pathogenesis of endometriosis in ESCs were evaluated using estradiol, tumor necrosis factor alpha (TNF-α), interleukin 1β (IL-1β), and IL-32, administered alone or in combination with DNG. Implanted endometrial tissues were compared between C57BL/6 mice that did or did not receive DNG treatment by using size measurements and immunohistochemistry. A significant decrease in cell viability, protein kinase B (AKT) phosphorylation, and the expression of p21-activated kinase 4 and vascular endothelial growth factor were observed in ESCs treated with estradiol plus DNG. Cell viability, AKT phosphorylation, and proliferating cell nuclear antigen (PCNA) expression also decreased significantly after TNF-α plus DNG treatment. Treatment with IL-1β or IL-32 plus DNG significantly decreased cell viability or PCNA expression, respectively. The size of the implanted endometrial tissue significantly decreased in mice treated with DNG, accompanied by decreased PCNA expression. Thus, DNG may reduce cell viability and proliferation induced by estradiol, TNF-α, IL-1β, and IL-32, and inhibit the endometriosis pathogenesis by decreasing PCNA expression.
Insights
Dienogest (DNG) reduces endometriosis cell viability and proliferation. This medication inhibits key markers associated with endometriosis, offering a potential therapeutic mechanism for the condition.
Area of Science:
- Gynecology
- Cell Biology
- Pharmacology
Background:
- Endometriosis is a condition affecting endometrial cells.
- Limited data exist on Dienogest's (DNG) mechanism of action.
- Investigating DNG's effects on endometrial stromal cells (ESCs) is crucial.
Purpose of the Study:
- To investigate DNG's biological effects on human ESCs.
- To evaluate DNG's impact on endometriosis-related markers.
- To assess DNG's efficacy in in vivo and in vitro models.
Main Methods:
- In vitro studies using ESCs treated with estradiol, TNF-α, IL-1β, IL-32, and DNG.
- In vivo studies using C57BL/6 mice with implanted endometrial tissues.
- Analysis of cell viability, protein kinase B (AKT) phosphorylation, PCNA, and tissue size.
Main Results:
- DNG decreased cell viability, AKT phosphorylation, and specific protein expression (p21-activated kinase 4, VEGF) with estradiol.
- DNG reduced cell viability, AKT phosphorylation, and PCNA expression with TNF-α.
- DNG decreased cell viability or PCNA expression with IL-1β or IL-32, respectively.
- DNG treatment reduced implanted endometrial tissue size and PCNA expression in mice.
Conclusions:
- Dienogest reduces cell viability and proliferation induced by various factors.
- DNG inhibits endometriosis pathogenesis by decreasing PCNA expression.
- DNG demonstrates therapeutic potential in endometriosis treatment.
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