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首页> 外文期刊>American journal of reproductive immunology : >Puerarin attenuates preeclampsia-induced trophoblast mobility loss and inflammation by modulating miR-181b-5p/RBAKaxis
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Puerarin attenuates preeclampsia-induced trophoblast mobility loss and inflammation by modulating miR-181b-5p/RBAKaxis

机译:通过调节miR-181b-5p/rbakaxis

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Problem: Preeclampsia (PE) is a serious pregnancy complication characterized by inflammation and impaired trophoblast motility. Puerarin (Pue) is a functional compound with anti-PE potential. The current study aimed to explore the therapeutic effects of Pue on PE as well as the associated mechanism by focusing on the interaction between Pue and microRNAs (miRs). Methods of study: Human villous trophoblast HTR-8/SVneo cells were treated with TNF-α and Pue, and a change in miR expression profile was determined. The anti-PE effects of Pue were validated in rat models by measuring blood pressure, 24-h pro-teinuria, and cytokine levels. The mechanism was explored by focusing on miR-181b-5p/RBAKaxis. Results: The induction of PE increased blood pressure and 24-h proteinuria, and induced TNF-α, IL-1β, and IL-6 levels, which was reversed by Pue. In in vitro assays, TNF-α suppressed viability, induced apoptosis and inflammatory response, and inhibited migration in trophoblasts, which was attenuated by Pue. At molecular level, the expression level of miR- 181b-5p was both induced in vivo and in vitro with the development of PE symptoms, contributing to the inhibited expression of RBAK. The induced expression of miR-181b-5p under Pue treatment showed that the reinduction of miR-181b-5p counteracted the effects of Pue, indicating the key role of the miR in the protective effects of Pue against PE. Conclusions: The current study verified the anti-PE function of Pue: the compound suppressed inflammatory response associated with PE, and improved trophoblast motility. The effects depended on the inhibition of miR-181b-5p that inhibited the expression of RBAK.
机译:问题:先兆子痫(PE)是一种严重的妊娠并发症,其特征是炎症和滋养细胞运动受损。 Puerarin(PUE)是具有抗PE电位的功能化合物。当前的研究旨在通过关注PUE和microRNA之间的相互作用(miRS)来探索PUE对PE以及相关机制的治疗作用。研究方法:用TNF-α和PUE处理人绒毛细胞HTR-8/SVNEO细胞,并确定miR表达谱的变化。通过测量血压,24小时pro-Techinuria和细胞因子水平,在大鼠模型中验证了PUE的抗PE效应。通过关注miR-181b-5p/rbakaxis来探索该机制。结果:PE的诱导增加了血压和24小时蛋白尿,以及诱导的TNF-α,IL-1β和IL-6水平,这被PUE逆转。在体外测定中,TNF-α抑制了生存力,诱导的凋亡和炎症反应,并抑制了滋养细胞的迁移,这被PUE减弱。在分子水平上,在体内和体外诱导miR-181b-5p的表达水平随着PE症状的发展而诱导,从而导致RBAK的抑制表达。在PUE处理下诱导的miR-181b-5p表达表明,MiR-181b-5p的重新诱导抵消了PUE的作用,表明MIR在PUE对PE的保护作用中的关键作用。结论:当前的研究验证了PUE的抗PE功能:化合物抑制了与PE相关的炎症反应,并改善了滋养细胞的运动。该作用取决于抑制RBAK表达的miR-181b-5p的抑制。

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