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核因子-κB:子宫内膜异位症病理生理学中炎症和细胞存活的主要调节因子。

Nuclear factor-kappaB: a main regulator of inflammation and cell survival in endometriosis pathophysiology.

机构信息

Instituto de Investigaciones Materno Infantil, Departamento de Obstetricia y Ginecología, Hospital Clínico San Borja-Arriarán, Facultad de Medicina, Universidad de Chile, Santiago, Chile.

出版信息

Fertil Steril. 2012 Sep;98(3):520-8. doi: 10.1016/j.fertnstert.2012.06.021. Epub 2012 Jul 6.

DOI:10.1016/j.fertnstert.2012.06.021
PMID:22771029
Abstract

OBJECTIVE

To update, analyze, and summarize the literature concerning nuclear factor-kappaB (NF-κB) participation in endometriosis pathophysiology.

DESIGN

Review.

RESULT(S): Nuclear factor-kappaB is physiologically activated in the human endometrium, showing variable activity. A cyclic p65-DNA binding pattern was shown in the endometrium of healthy women. This cyclic pattern was altered in the endometrium of patients with endometriosis. Nuclear factor-kappaB is basally activated in peritoneal endometriotic lesions, showing higher p65 activity in red endometriotic lesions than in black lesions. In vivo and in vitro studies show up-regulation of inflammation and cell proliferation and down-regulation of apoptosis by NF-κB activity. Iron overload has been shown in the pelvic cavity of endometriosis patients, and iron overload and oxidative stress activate NF-κB in macrophages, which have been shown to participate in the endometriosis-associated inflammatory reaction.

CONCLUSION(S): Nuclear factor-kappaB activation dysregulation in the endometrium of endometriosis patients may explain some endometrial biological alterations associated with endometriosis. The scientific evidence strongly suggests that NF-κB activity in endometriotic cells stimulates inflammation and cell proliferation and inhibits apoptosis, favoring the development and maintenance of endometriosis. Iron overload in the pelvic cavity of endometriosis patients could be a main factor enhancing oxidative stress and activating NF-κB in a chronic manner, contributing to endometriosis establishment and growth.

摘要

目的

更新、分析和总结核因子-κB(NF-κB)参与子宫内膜异位症病理生理学的文献。

设计

综述。

结果

NF-κB 在人类子宫内膜中生理性激活,表现出不同的活性。健康女性子宫内膜中显示出 p65-DNA 结合的周期性模式。这种周期性模式在子宫内膜异位症患者的子宫内膜中发生了改变。腹膜子宫内膜异位症病变中 NF-κB 呈基础激活状态,红色子宫内膜异位症病变中的 p65 活性高于黑色病变。体内和体外研究表明 NF-κB 活性可上调炎症和细胞增殖,下调细胞凋亡。已在子宫内膜异位症患者的盆腔中发现铁过载,铁过载和氧化应激可激活巨噬细胞中的 NF-κB,巨噬细胞已被证明参与了与子宫内膜异位症相关的炎症反应。

结论

子宫内膜异位症患者子宫内膜中 NF-κB 的激活失调可能解释了一些与子宫内膜异位症相关的子宫内膜生物学改变。科学证据强烈表明,子宫内膜异位症细胞中 NF-κB 的活性刺激炎症和细胞增殖,抑制细胞凋亡,有利于子宫内膜异位症的发生和维持。子宫内膜异位症患者盆腔中的铁过载可能是增强氧化应激和慢性激活 NF-κB 的主要因素,有助于子宫内膜异位症的建立和生长。

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