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首页> 外文期刊>Progress in Artificial Intelligence >De-Glycyrrhizinated Licorice Extract Attenuates High Glucose-Stimulated Renal Tubular Epithelial-Mesenchymal Transition via Suppressing the Notch2 Signaling Pathway
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De-Glycyrrhizinated Licorice Extract Attenuates High Glucose-Stimulated Renal Tubular Epithelial-Mesenchymal Transition via Suppressing the Notch2 Signaling Pathway

机译：De-Glycyrhizinated甘草提取物通过抑制Notch2信号通路抑制高葡萄糖刺激的肾小管上皮 - 间充质转换

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Tubulointerstitial fibrosis is a major pathological hallmark of diabetic nephropathy. Increasing evidence has shown that epithelial-to-mesenchymal transition (EMT) of renal proximal tubular cells plays a crucial role in tubulointerstitial fibrosis. Herein, we aimed to elucidate the detailed mechanism of EMT in renal tubular cells under high glucose (HG) conditions, and to investigate the potential of licorice, a medicinal herb, to inhibit HG-induced EMT. Our results showed that renal tubular epithelial cells (normal rat kidney cell clone 52E; NRK-52E) exposed to HG resulted in EMT induction characterized by increased fibronectin and alpha-SMA (alpha-smooth muscle actin) but decreased E-cadherin. Elevated levels of cleaved Notch2, MAML-1 (mastermind-like transcriptional coactivator 1), nicastrin, Jagged-1 and Delta-like 1 were also concomitantly detected in HG-cultured cells. Importantly, pharmacological inhibition, small interfering RNA (siRNA)-mediated depletion or overexpression of the key components of Notch2 signaling in NRK-52E cells supported that the activated Notch2 pathway is essential for tubular EMT. Moreover, we found that licorice extract (LE) with or without glycyrrhizin, one of bioactive components in licorice, effectively blocked HG-triggered EMT in NRK-52E cells, mainly through suppressing the Notch2 pathway. Our findings therefore suggest that Notch2-mediated renal tubular EMT could be a therapeutic target in diabetic nephropathy, and both LE and de-glycyrrhizinated LE could have therapeutic potential to attenuate renal tubular EMT and fibrosis.
机译：微管膨胀性纤维化是糖尿病肾病的主要病态标志。越来越多的证据表明，肾近端管状细胞的上皮 - 间充质转换（EMT）在细胞间隔纤维化中起着至关重要的作用。在此，我们旨在阐明高葡萄糖（Hg）条件下肾小管细胞EMT在肾小管细胞中的详细机制，并研究甘草的潜力，一种药草，抑制HG诱导的EMT。我们的研究结果表明，肾小管上皮细胞（正常大鼠肾细胞克隆52E; NRK-52E）暴露于HG导致EMT诱导，其特征在于纤连蛋白和α-SMA（α-平滑肌肌动蛋白）但含量降低。在HG培养的细胞中也伴随着升高的切割Notch2，MAML-1（类似蛋白酶样转录剂1），尼卡斯汀，锯齿状-1和δ状1。重要的是，在NRK-52E细胞中，在NRK-52E细胞中的NRCH2信号传导的关键部件的药理抑制，小干扰RNA（siRNA）介导的耗尽或过表达支持，所述活性的Notch2途径对于管状EMT是必不可少的。此外，我们发现甘草提取物（Le）与甘草中的生物活性组分之一，有效地阻断了NRK-52E细胞中的HG触发的EMT，主要是通过抑制Notch2途径。因此，我们的研究结果表明，Notch2介导的肾小管EMT可以是糖尿病肾病的治疗靶标，并且Le和De-Glycyrhizinated的Le可以具有治疗潜力来减弱肾小管EMT和纤维化。

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