众所周知，子宫内膜异位症是一种慢性炎症性疾病。子宫内膜异位症的发生在很大程度上受到雌激素受体 β (ERβ) 的影响，而 NOD 样受体 (NLR) 家族 CARD 结构域 5 (NLRC5) 在子宫内膜异位症期间表现出抗炎特性。然而，NLRC5介导的抗炎作用是否参与ERβ介导的子宫内膜异位症仍不确定。本研究旨在评估这种关系。收集了9例子宫内膜异位症患者的在位子宫内膜组织和10例异位子宫内膜组织，并分析了10例健康生育女性的子宫内膜样本，并使用免疫组织化学法定量了ERβ的表达水平。免疫组化）。随后，我们通过腹腔注射构建子宫内膜异位症小鼠模型。我们检测了子宫内膜异位症小鼠中ERβ、NLRC5、肿瘤坏死因子-α（TNF-α）、白细胞介素（IL）-6和IL-10的表达，并测量了异位病变的体积。在体外，分别用过表达ERβ和过表达NLRC5的质粒转染人子宫内膜基质细胞（hESC）。然后，我们使用定量实时 PCR (qRT-PCR) 和蛋白质印迹分析评估了 ERβ 和 NLRC5 的表达。此外，我们通过酶联免疫吸附测定（ELISA）测量了细胞培养上清液中TNF-α、IL-6和IL-10的浓度。此外，我们使用transwell和伤口愈合实验评估了hESC的迁移和侵袭能力。抑制NLRC5表达可促进子宫内膜异位症小鼠异位病变的发展，上调促炎因子TNF-α和IL-6的表达，并促进子宫内膜异位症小鼠异位病变的发展。下调抗炎因子IL-10的表达。 NLRC5在子宫内膜异位症中的高表达依赖于ERβ的过表达。而ERβ促进hESCs迁移部分依赖于炎症微环境。最后，NLRC5过表达抑制了ERβ介导的子宫内膜异位症的发展和炎症反应。我们的研究结果表明，先天性免疫分子NLRC5介导的抗炎参与了ERβ介导的子宫内膜异位症的发展，并部分阐明了子宫内膜异位症的病理机制，扩大了我们对子宫内膜异位症的认识。与子宫内膜异位症炎症反应相关的特定分子，并可能为子宫内膜异位症提供新的治疗靶点。© 2024。作者。

Endometriosis is well known as a chronic inflammatory disease. The development of endometriosis is heavily influenced by the estrogen receptor β (ERβ), while NOD-like receptors (NLRs) family CARD domain-containing 5 (NLRC5) exhibits anti-inflammatory properties during endometriosis. However, whether NLRC5-mediated anti-inflammation is involved in the ERβ-mediated endometriosis is still uncertain. This study aimed to assess that relation.Nine cases of eutopic endometrial tissue and ten cases of ectopic endometrial tissue were collected from patients with endometriosis, and endometrial samples from ten healthy fertile women were analyzed, and the expression levels of ERβ were quantified using immunohistochemistry (IHC). Subsequently, we constructed mouse model of endometriosis by intraperitoneal injection. We detected the expression of ERβ, NLRC5, tumor necrosis factor-alpha (TNF-α), interleukin (IL)-6, and IL-10 and measured the volume of ectopic lesions in mice with endometriosis. In vitro, human endometrial stromal cells (hESCs) were transfected respectively with ERβ-overexpressing and NLRC5-overexpressing plasmids. We then assessed the expression of ERβ and NLRC5 using quantitative real-time PCR (qRT-PCR) and western blot analysis. Furthermore, we measured the concentrations of TNF-α, IL-6, and IL-10 in the cell culture supernatant through enzyme-linked immunosorbent assay (ELISA). Additionally, we evaluated the migration and invasion ability of hESCs using transwell and wound healing assays.Inhibition of NLRC5 expression promotes the development of ectopic lesions in mice with endometriosis, upregulates the expression of pro-inflammatory factors TNF-α and IL-6, and downregulates the expression of anti-inflammatory factor IL-10. The high expression of NLRC5 in endometriosis depended on the ERβ overexpression. And ERβ promoted the migration of hESCs partially depend on inflammatory microenvironment. Lastly, NLRC5 overexpression inhibited ERβ-mediated development and inflammatory response of endometriosis.Our results suggest that the innate immune molecule NLRC5-mediated anti-inflammation participates in ERβ-mediated endometriosis development, and partly clarifies the pathological mechanism of endometriosis, expanding our knowledge of the specific molecules related to the inflammatory response involved in endometriosis and potentially providing a new therapeutic target for endometriosis.© 2024. The Author(s).