Progestin suppressed inflammation and cell viability of tumor necrosis factor‐α‐stimulated endometriotic stromal cells
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Progestins including dienogest, norethisterone acetate, and medroxyprogesterone acetate suppressed inflammation and cell viability in TNF-α-stimulated endometriotic stromal cells.
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Abstract
PROBLEM: Endometriosis is an estrogen-dependent inflammatory disease. Progestins are a first-line treatment for endometriosis via activation of pituitary progesterone receptors and suppression of systemic estrogen: a less than optimal treatment. Increasing evidence is beginning to show that progestins may also influence local endometriotic cells, which may contribute to their clinical efficacy. METHOD OF STUDY: Endometrial stromal cells (ESC) isolated from women with endometriosis were cultured with TNF-α to simulate an inflammatory environment. ESC were treated with the progestins, medroxyprogesterone acetate (MPA), norethisterone acetate (NETA), or dienogest (DNG) and cytokine mRNA production, protein secretion, and cell viability measured. RESULTS: DNG, NETA, and MPA suppressed the secretion of interleukin (IL)-6, IL-8, and monocyte chemotactic protein (MCP)-1 from ESC. DNG and NETA only reduced the TNF-α-stimulated mRNA production. All three progestins suppressed TNF-α-stimulated ESC proliferation. CONCLUSION: Progestins may influence endometriotic stromal cells altering the inflammatory microenvironment and their clinical efficacy.
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- In vivo effects of AZD4547, a novel fibroblast growth factor receptor inhibitor, in a mouse model of endometriosis 2021
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- Comparison of dienogest effects upon 3,3′–diindolylmethane supplementation in models of endometriosis and clinical cases 2018
- Placenta previa and placental abruption after assisted reproductive technology in patients with endometriosis: a systematic review and meta-analysis 2018
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