Agents Blocking the Nuclear Factor-κB Pathway Are Effective Inhibitors of Endometriosis in an in vivo Experimental Model

Reinaldo González-Ramos, Anne Van Langendonckt, Sylvie Defrère, Jean‐Christophe Lousse, Jean-Christophe Lousse, Marcel Mettlen, Alain Guillet, Jacques Donnez
Gynecologic and obstetric investigation · 2007 · vol. 65(3) , pp. 174–186 · doi:10.1159/000111148 · PMID:18025832 · W2063553906
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NF-κB inhibitors reduced endometriotic lesion development in mice by decreasing ICAM-1 expression and cell proliferation while increasing apoptosis.

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Abstract

BACKGROUND: In vitro studies suggest that the transcription factor nuclear factor-kappa B (NF-kappaB) is implicated in the transduction of proinflammatory signals in endometriosis. The aim of this study was to investigate the involvement of NF-kappaB and the processes regulated by NF-kappaB in the initial development of endometriotic lesionsin vivo. METHODS: Endometriosis was induced in nude mice by intraperitoneal injection of fluorescent-labeled menstrual endometrium. Two NF-kappaB inhibitors (BAY 11-7085 and SN-50) were injected intraperitoneally on days 0, 2 and 4 after endometriosis induction, and endometriotic lesions were recovered on day 5. Number, mass, fluorimetry and surface (morphometry) of endometriotic lesions were quantified. NF-kappaB activation, intercellular adhesion molecule (ICAM)-1 expression, cell proliferation and apoptosis were evaluated by immunohistochemical analyses and the TUNEL method. RESULTS: Both NF-kappaB inhibitors induced a significant reduction in lesion development compared to control mice. NF-kappaB activation and ICAM-1 expression of endometriotic lesions were significantly reduced in treated mice, and cell proliferation was significantly reduced in BAY 11-7085-treated mice. Both inhibitors produced a significant increase in apoptosis of endometriotic lesions, as assessed by active caspase-3 immunostaining and the TUNEL method. CONCLUSION: This study demonstrates, for the first time, that the NF-kappaB pathway is implicated in the development of endometriotic lesions in vivo and that NF-kappaB inhibition reduces ICAM-1 expression and cell proliferation, but increases apoptosis of endometriotic lesions, diminishing the initial development of endometriosis in an animal model.

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Condition tags

endometriosis

MeSH descriptors

Endometriosis Enzyme Inhibitors NF-kappa B Nitriles Peptides Sulfones Animals Apoptosis Apoptosis Cell Proliferation Cell Proliferation Disease Models, Animal Endometriosis Endometriosis Enzyme Inhibitors Female Humans Intercellular Adhesion Molecule-1 Intercellular Adhesion Molecule-1 Mice

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