Low-dose SKA Progesterone and Interleukin-10 modulate the inflammatory pathway in endometriotic cell lines

Mancini F; Francesca Mancini; Domenico Milardi; Carfagna P; Piero Carfagna; Giuseppe Grande; Vincenzo Miranda; Alessandra De Cicco Nardone; Alessandra Nardone; De Cicco Nardone A; Ricciardi D; Domenico Ricciardi; Alfredo Pontecorvi; Marana R; Riccardo Marana; De Cicco Nardone F; Fiorenzo De Cicco Nardone

doi:10.1016/j.intimp.2017.12.008

Low-dose SKA Progesterone and Interleukin-10 modulate the inflammatory pathway in endometriotic cell lines

Mancini F, Francesca Mancini, Domenico Milardi, Carfagna P, Piero Carfagna, Giuseppe Grande, Vincenzo Miranda, Alessandra De Cicco Nardone, Alessandra Nardone, De Cicco Nardone A, Ricciardi D, Domenico Ricciardi, Alfredo Pontecorvi, Marana R, Riccardo Marana, De Cicco Nardone F, Fiorenzo De Cicco Nardone

International Immunopharmacology · 2017 · vol. 55 , pp. 223–230 · doi:10.1016/j.intimp.2017.12.008 · PMID:29272819 · W2781234735

Other OA: closed CC0 ⤵ 4 in-corpus citations

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⚙ AI-generated summary by gemini-2.5-flash-lite, 2026-06-28 ⓘ

This study investigated how low-dose SKA progesterone and IL-10 affect the inflammatory pathway within endometriotic cell lines.

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Condition tags

endometriosis

MeSH descriptors

Immunologic Factors Interleukin-10 Progesterone Cell Line Cell Line Endometriosis Endometriosis Endometriosis Endometriosis Female Female Humans Humans Immunologic Factors Immunologic Factors Interleukin-10 Interleukin-10 Progesterone Progesterone Signal Transduction

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References (50)

Agents blocking the nuclear factor-kappaB pathway are effective inhibitors of endometriosis in an in vivo experimental model via openalex
Application of the nuclear factor-kappaB inhibitor BAY 11-7085 for the treatment of endometriosis: an in vitro study via openalex
Cervical mucus proteome in endometriosis via openalex
Clinical management of endometriosis via openalex
Clinical Management of Endometriosis via openalex
Current place of progestins in the treatment of endometriosis-related complaints via openalex
Dienogest, a synthetic progestin, inhibits prostaglandin E2 production and aromatase expression by human endometrial epithelial cells in a spheroid culture system via openalex
[Endometriosis: the gynecologist's opinion] via openalex
Estrogen metabolizing enzymes in endometrium and endometriosis via openalex
Expression and regulation of estrogen-converting enzymes in ectopic human endometrial tissue via openalex
Identification of an invasive, N-cadherin-expressing epithelial cell type in endometriosis using a new cell culture model via openalex
Increased activation of nuclear factor-kappa B (NF-kappaB) in isolated peritoneal macrophages of patients with endometriosis via openalex
Inflammation and endometriosis via openalex
Inflammatory status influences aromatase and steroid receptor expression in endometriosis via openalex
Insights into iron and nuclear factor-kappa B (NF-kappaB) involvement in chronic inflammatory processes in peritoneal endometriosis via openalex
Involvement of nuclear factor-kappaB in macrophage migration inhibitory factor gene transcription up-regulation induced by interleukin- 1 beta in ectopic endometrial cells via openalex
Involvement of the nuclear factor-κB pathway in the pathogenesis of endometriosis via openalex
Lipopolysaccharide-promoted proliferation of endometriotic stromal cells via induction of tumor necrosis factor alpha and interleukin-8 expression via openalex
Mechanisms of excessive estrogen formation in endometriosis via openalex
Nuclear factor-kappa B is constitutively activated in peritoneal endometriosis via openalex
Nuclear factor-kappab (NF-kappaB): an unsuspected major culprit in the pathogenesis of endometriosis that is still at large? via openalex
Peroxisome proliferator-activated receptor-gamma ligand reduced tumor necrosis factor-alpha-induced interleukin-8 production and growth in endometriotic stromal cells via openalex
Progesterone and progestational compounds attenuate tumor necrosis factor alpha-induced interleukin-8 production via nuclear factor kappa B inactivation in endometriotic stromal cells via openalex
Progestogens for endometriosis: forward to the past via openalex
Prokineticin 1, homeobox A10, and progesterone receptor messenger ribonucleic acid expression in primary cultures of endometrial stromal cells isolated from endometrium of healthy women and from eutopic endometrium of women with endometriosis via openalex
Reduction of apoptosis and proliferation in endometriosis via openalex
Selective inhibition of prostaglandin E2 receptors EP2 and EP4 induces apoptosis of human endometriotic cells through suppression of ERK1/2, AKT, NFkappaB, and beta-catenin pathways and activation of intrinsic apoptotic mechanisms via openalex
Stimulation of macrophage migration inhibitory factor expression in endometrial stromal cells by interleukin 1, beta involving the nuclear transcription factor NFkappaB via openalex
Sulindac suppresses nuclear factor-kappaB activation and RANTES gene and protein expression in endometrial stromal cells from women with endometriosis via openalex
Thalidomide inhibits tumor necrosis factor-alpha-induced interleukin-8 expression in endometriotic stromal cells, possibly through suppression of nuclear factor-kappaB activation via openalex
Tumor necrosis factor-alpha-induced interleukin-8 (IL-8) expression in endometriotic stromal cells, probably through nuclear factor-kappa B activation: gonadotropin-releasing hormone agonist treatment reduced IL-8 expression via openalex
Tumor necrosis factor-alpha induced the release of interleukin-6 from endometriotic stromal cells by the nuclear factor-kappaB and mitogen-activated protein kinase pathways via openalex
W6686818377 via openalex
W1993354065 via openalex
W2010311608 via openalex
W2030531265 via openalex
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W2065052724 via openalex
W2070263689 via openalex
W2074799394 via openalex
W2116022066 via openalex
W2127529986 via openalex
W2145719125 via openalex
W2148020952 via openalex
W2150548455 via openalex
W2157100128 via openalex
W2160329177 via openalex
W2185194462 via openalex
W2604749970 via openalex
W4211081176 via openalex

Cited by (4)

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License: CC0 · commercial use OK

[1] Agents blocking the nuclear factor-kappaB pathway are effective inhibitors of endometriosis in an in vivo experimental model via openalex

[2] Application of the nuclear factor-kappaB inhibitor BAY 11-7085 for the treatment of endometriosis: an in vitro study via openalex

[3] Cervical mucus proteome in endometriosis via openalex

[4] Clinical management of endometriosis via openalex

[5] Clinical Management of Endometriosis via openalex

[6] Current place of progestins in the treatment of endometriosis-related complaints via openalex

[7] Dienogest, a synthetic progestin, inhibits prostaglandin E2 production and aromatase expression by human endometrial epithelial cells in a spheroid culture system via openalex

[8] [Endometriosis: the gynecologist's opinion] via openalex

[9] Estrogen metabolizing enzymes in endometrium and endometriosis via openalex

[10] Expression and regulation of estrogen-converting enzymes in ectopic human endometrial tissue via openalex

[11] Identification of an invasive, N-cadherin-expressing epithelial cell type in endometriosis using a new cell culture model via openalex

[12] Increased activation of nuclear factor-kappa B (NF-kappaB) in isolated peritoneal macrophages of patients with endometriosis via openalex

[13] Inflammation and endometriosis via openalex

[14] Inflammatory status influences aromatase and steroid receptor expression in endometriosis via openalex

[15] Insights into iron and nuclear factor-kappa B (NF-kappaB) involvement in chronic inflammatory processes in peritoneal endometriosis via openalex

[16] Involvement of nuclear factor-kappaB in macrophage migration inhibitory factor gene transcription up-regulation induced by interleukin- 1 beta in ectopic endometrial cells via openalex

[17] Involvement of the nuclear factor-κB pathway in the pathogenesis of endometriosis via openalex

[18] Lipopolysaccharide-promoted proliferation of endometriotic stromal cells via induction of tumor necrosis factor alpha and interleukin-8 expression via openalex

[19] Mechanisms of excessive estrogen formation in endometriosis via openalex

[20] Nuclear factor-kappa B is constitutively activated in peritoneal endometriosis via openalex

[21] Nuclear factor-kappab (NF-kappaB): an unsuspected major culprit in the pathogenesis of endometriosis that is still at large? via openalex

[22] Peroxisome proliferator-activated receptor-gamma ligand reduced tumor necrosis factor-alpha-induced interleukin-8 production and growth in endometriotic stromal cells via openalex

[23] Progesterone and progestational compounds attenuate tumor necrosis factor alpha-induced interleukin-8 production via nuclear factor kappa B inactivation in endometriotic stromal cells via openalex

[24] Progestogens for endometriosis: forward to the past via openalex

[25] Prokineticin 1, homeobox A10, and progesterone receptor messenger ribonucleic acid expression in primary cultures of endometrial stromal cells isolated from endometrium of healthy women and from eutopic endometrium of women with endometriosis via openalex

[26] Reduction of apoptosis and proliferation in endometriosis via openalex

[27] Selective inhibition of prostaglandin E2 receptors EP2 and EP4 induces apoptosis of human endometriotic cells through suppression of ERK1/2, AKT, NFkappaB, and beta-catenin pathways and activation of intrinsic apoptotic mechanisms via openalex

[28] Stimulation of macrophage migration inhibitory factor expression in endometrial stromal cells by interleukin 1, beta involving the nuclear transcription factor NFkappaB via openalex

[29] Sulindac suppresses nuclear factor-kappaB activation and RANTES gene and protein expression in endometrial stromal cells from women with endometriosis via openalex

[30] Thalidomide inhibits tumor necrosis factor-alpha-induced interleukin-8 expression in endometriotic stromal cells, possibly through suppression of nuclear factor-kappaB activation via openalex

[31] Tumor necrosis factor-alpha-induced interleukin-8 (IL-8) expression in endometriotic stromal cells, probably through nuclear factor-kappa B activation: gonadotropin-releasing hormone agonist treatment reduced IL-8 expression via openalex

[32] Tumor necrosis factor-alpha induced the release of interleukin-6 from endometriotic stromal cells by the nuclear factor-kappaB and mitogen-activated protein kinase pathways via openalex

[33] W6686818377 via openalex

[34] W1993354065 via openalex

[35] W2010311608 via openalex

[36] W2030531265 via openalex

[37] W2047320556 via openalex

[38] W2065052724 via openalex

[39] W2070263689 via openalex

[40] W2074799394 via openalex

[41] W2116022066 via openalex

[42] W2127529986 via openalex

[43] W2145719125 via openalex

[44] W2148020952 via openalex

[45] W2150548455 via openalex

[46] W2157100128 via openalex

[47] W2160329177 via openalex

[48] W2185194462 via openalex

[49] W2604749970 via openalex

[50] W4211081176 via openalex