Inflammation and oxidative stress are involved in the pathogenesis of preeclampsia. Therefore, the aim of this study was to investigate the expression of Toll-like receptor (TLR) (TLR-4, HMGB1, NFκB, IκBα) and hypoxic (HIF-1α, HIF-1β, PHD, pVHL) pathway proteins in the placenta of preeclamptic pregnant women after 28 weeks of gestational period. A possible association between these 2 pathways was also explored. A total of 194 placental tissues of preeclamptic as well as healthy pregnant women were analyzed by immunohistochemistry. On the basis of gestational age, the samples were divided into 2 groups, I (28-36 wk) and II (36 wk onwards), with 55 and 139 samples in the respective groups. The expression of both TLR (TLR-4, HMGB1, NFκB, IκBα) and hypoxic (HIF-1α, HIF-1β, PHD, pVHL) pathway proteins were significantly modulated in the placental tissues of preeclampsia as compared with control. The 2 pathways were interlinked in preeclampsia. This study highlights the intercorrelation of both TLR and hypoxic signalling pathways that may be a causative factor for the pathophysiology of preeclampsia.

中文翻译：

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先兆子痫病因学中 Toll 样受体与缺氧信号传导的融合。

炎症和氧化应激参与先兆子痫的发病机制。因此，本研究的目的是研究Toll样受体（TLR）（TLR-4、HMGB1、NFκB、IκBα）和缺氧（HIF-1α、HIF-1β、PHD、pVHL）通路蛋白在先兆子痫孕妇妊娠 28 周后的胎盘。还探讨了这两条途径之间可能的关联。对 194 例先兆子痫和健康孕妇的胎盘组织进行了免疫组织化学分析。根据孕龄，将样本分为I组（28-36周）和II组（36周以上），各组各有55个样本和139个样本。TLR（TLR-4、HMGB1、NFκB、IκBα）和缺氧（HIF-1α、HIF-1β、PHD、与对照相比，先兆子痫胎盘组织中 pVHL）途径蛋白受到显着调节。在先兆子痫中这两条途径是相互关联的。这项研究强调了 TLR 和缺氧信号通路的相互关联，这可能是先兆子痫病理生理学的致病因素。