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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Condition tags

endometriosis

MeSH descriptors

Endometriosis Endometrium Inflammation Progestins Stromal Cells Cell Proliferation Cells, Cultured Cell Survival Cellular Microenvironment Cytokines Cytokines Cytokines Endometriosis Endometrium Estrogens Estrogens Female Humans Immunosuppression Therapy Inflammation

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europepmc
last seen: 2026-06-11T06:19:48.454388+00:00
openalex
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