已证实子宫内膜异位症(EMs)的发病机制与免疫、细胞凋亡、激素水平异常等因素相关。核转录因子κB(NF-κB)在正常情况下与其负调控蛋白结合处于失活状态,当细胞接受外来刺激后这种结合被破坏,活化的NF-κB与其靶基因启动子结合后促进基因表达。NF-κB的靶基因产物中有许多与炎症反应、细胞凋亡、激素合成相关分子,并且部分靶基因产物可以激活NF-κB,从而形成一条正反馈途径,使NF-κB及其靶基因产物的生物学效应得到放大。NF-κB可能通过其靶基因直接或间接地参与EMs发病。 It has been confirmed that the pathogenesis of endometriosis (EMs) is associated with immune, apoptosis, abnormal hormone levels and other factors. Nuclear factor-kappa B (NF-κB) is normally inactivated by binding to its negative regulatory protein, which is disrupted when cells are exposed to external stimuli. Activation of NF-κB promotes gene expression by binding to its target gene promoter . Many of the target gene products of NF-κB are involved in inflammation, apoptosis and hormone synthesis, and some target gene products can activate NF-κB, thus forming a positive feedback pathway that makes NF-κB and its target gene products The biological effect is amplified. NF-κB may participate in the pathogenesis of EMs directly or indirectly through its target gene.