Department of Obstetrics and Gynaecology, University of Melbourne, Mercy Hospital for Women, Heidelberg, Melbourne, VIC 3084, Australia.
Oxid Med Cell Longev. 2013;2013:485201. doi: 10.1155/2013/485201. Epub 2013 Jun 5.
Infection/inflammation is commonly associated with preterm birth (PTB), initiating uterine contractions and rupture of fetal membranes. Proinflammatory cytokines induce matrix metalloproteinases (MMPs) that degrade the extracellular matrix (ECM) and prostaglandins which initiate uterine contractions. Nuclear factor-κB (NF-κB) and activator-protein- (AP-)1 have key roles in the formation of these prolabour mediators. In nongestational tissues, dietary flavonoids such as luteolin and kaempferol inhibit NF-κB, AP-1, and their downstream targets. The aim of this study was to determine if luteolin and kaempferol reduce infection-induced prolabour mediators in human gestational tissues. Fetal membranes were incubated with LPS, and primary amnion cells and myometrial cells were incubated with IL-1β in the absence or presence of luteolin or kaempferol. Luteolin and kaempferol significantly reduced LPS-induced secretion of proinflammatory cytokines (IL-6 and IL-8) and prostaglandins (PGE(2) and PGF(2α)) in fetal membranes, IL-1β-induced COX-2 gene expression and prostaglandin production in myometrium, and IL-1β-induced MMP-9 activity in amnion and myometrial cells. Luteolin and kaempferol decreased IL-1β-induced NF-κB p65 DNA binding activity and nuclear c-Jun expression. In conclusion, luteolin and kaempferol inhibit prolabour mediators in human gestational tissues. Given the central role of inflammation in provoking preterm labour, phytophenols may be a therapeutic approach to reduce the incidence of PTB.
感染/炎症通常与早产(PTB)相关,引发子宫收缩和胎膜破裂。促炎细胞因子诱导基质金属蛋白酶(MMPs)降解细胞外基质(ECM)和前列腺素,引发子宫收缩。核因子-κB(NF-κB)和激活蛋白-1(AP-1)在这些促分娩介质的形成中起着关键作用。在非妊娠组织中,膳食类黄酮,如木樨草素和山奈酚,可抑制 NF-κB、AP-1 及其下游靶点。本研究旨在确定木樨草素和山奈酚是否能减少人妊娠组织中感染诱导的促分娩介质。用 LPS 孵育胎膜,用 IL-1β 孵育原代羊膜细胞和子宫平滑肌细胞,同时存在或不存在木樨草素或山奈酚。木樨草素和山奈酚可显著降低 LPS 诱导的胎膜促炎细胞因子(IL-6 和 IL-8)和前列腺素(PGE(2)和 PGF(2α))的分泌,IL-1β 诱导的子宫平滑肌细胞 COX-2 基因表达和前列腺素产生,以及 IL-1β 诱导的羊膜和子宫平滑肌细胞 MMP-9 活性。木樨草素和山奈酚降低了 IL-1β 诱导的 NF-κB p65 DNA 结合活性和核 c-Jun 表达。总之,木樨草素和山奈酚抑制人妊娠组织中的促分娩介质。鉴于炎症在引发早产中的核心作用,植物酚类可能是一种减少 PTB 发生率的治疗方法。