ERB-041, a selective ER beta agonist, inhibits iNOS production in LPS-activated peritoneal macrophages of endometriosis via suppression of NF-kappaB activation

Wang Xiu-li, Xiuli Wang, Xiu-li W, Cheng Wen-jun, Wen-jun C, Wenjun Cheng, Huihua Dai, Hui-hua D, Dai Hui-hua, Han Su-ping, Su-ping H, Suping Han, Fu Shi-long, Shi-long F, Shilong Fu
Molecular immunology · 2009 · vol. 46(11-12) , pp. 2413–2418 · doi:10.1016/j.molimm.2009.04.014 · PMID:19447495 · W2062557757
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ERB-041, a selective ERβ agonist, was found to inhibit inducible nitric oxide synthase (iNOS) production in lipopolysaccharide (LPS)-activated peritoneal macrophages from endometriosis patients by suppressing NF-κB activation.

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Abstract

OBJECTIVE: The aim of the present study was to assess the anti-inflammatory effects of selective ER beta (ER beta) agonist on lipopolysaccharide (LPS)-induced inducible nitric oxide synthase (iNOS) production in peritoneal macrophages (PMs) of endometriosis (EMS). METHODS: ER alpha (ER alpha) and ER beta expressions in PMs were analyzed by RT-PCR and immunoblot. The PMs of endometriosis were exposed to increasing concentrations of ER beta agonist ERB-041 over a period from 0.5 to 8h before stimulation with LPS and the levels of iNOS protein were evaluated by immunoblot. Subsequently, the PMs were pretreated with vehicle, ERB-041 or ER alpha agonist PPT before exposing to LPS. iNOS expression, p65 protein and active extracellular signal-regulated kinases (ERKs) level accumulated in the nuclear were detected by immunoblot. For experiment investigating the role of ERKs in LPS-induced iNOS expression, the PMs were pretreated with U0126, a specific ERK inhibitor, for 60 min before LPS treatment and iNOS expression was detected by immunoblot. RESULTS: The PMs of EMS expressed ER beta to a greater extent compared with normal women. Pretreatment the PMs with ERB-041 resulted in a significant inhibition of LPS-induced iNOS expression and NF-kappaB activation by preventing its nuclear translocation. The ERKs pathway was involved in the LPS-induced iNOS production and was not repressed by the activation of ERs. CONCLUSION: The inhibitory effect of ER beta agonist on LPS-induced iNOS production in PMs of EMS is likely mediated via repressing of nuclear factor-kappa B (NF-kappaB) but not ERKs signaling pathways.

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Condition tags

endometriosis

MeSH descriptors

Anti-Inflammatory Agents, Non-Steroidal Endometriosis Estrogen Receptor beta Macrophages, Peritoneal NF-kappa B Nitric Oxide Synthase Type II Oxazoles Anti-Inflammatory Agents, Non-Steroidal Anti-Inflammatory Agents, Non-Steroidal Cells, Cultured Cells, Cultured Endometriosis Endometriosis Endometriosis Endometriosis Estrogen Receptor beta Estrogen Receptor beta Estrogen Receptor beta Extracellular Signal-Regulated MAP Kinases Extracellular Signal-Regulated MAP Kinases

Citation neighborhood (2-hop)

Papers in the corpus that this work cites (lower rings, blue) and that cite this one (upper rings, green). Dot size scales with the paper's in-corpus citation count — bigger dot = more influential within the endo/adeno field. Click a dot to open that paper. Outer rings show 2-hop neighbours — papers reached through the immediate citers/citees. [ collapse to 1-hop ]

References (29)

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