PDF(Pubmed)
Abstract：
UNASSIGNED: Diabetic kidney disease (DKD) is a severe microvascular complication of diabetes mellitus that can lead to end-stage renal disease. Colquhounia root tablet (CRT) has shown therapeutic potential in treating DKD, but its efficacy and underlying mechanisms remain to be elucidated.
UNASSIGNED: A randomized controlled clinical trial was conducted on 61 DKD patients. The treatment group received CRT in addition to standard therapy, while the control group received standard therapy alone. Treatment efficacy and adverse events were evaluated after 3 months. Additionally, in vitro experiments using human renal tubular epithelial cells (HK-2) were performed to investigate the effect of CRT on high glucose (HG)-induced epithelial-mesenchymal transition (EMT) and the involvement of the PTEN/PI3K/AKT signaling pathway.
UNASSIGNED: CRT treatment significantly improved proteinuria and increased the effective treatment rate in DKD patients compared to the control group, with no significant difference in adverse events. Moreover, CRT reversed HG-induced EMT in HK-2 cells, as evidenced by the downregulation of α-SMA and upregulation of E-cadherin at both mRNA and protein levels. Mechanistically, CRT increased PTEN expression and inhibited the PI3K/AKT pathway, similar to the effects of the PI3K inhibitor LY29400. The combination of CRT and LY29400 further enhanced PTEN mRNA expression under HG conditions.
UNASSIGNED: CRT effectively improves proteinuria in DKD patients and ameliorates HG-induced EMT in HK-2 cells. The underlying mechanism may involve the upregulation of PTEN and subsequent inhibition of the PI3K/AKT signaling pathway. These findings provide new insights into the therapeutic potential of CRT for DKD treatment.
UNASSIGNED: A randomized controlled clinical trial was conducted on 61 DKD patients. The treatment group received CRT in addition to standard therapy, while the control group received standard therapy alone. Treatment efficacy and adverse events were evaluated after 3 months. Additionally, in vitro experiments using human renal tubular epithelial cells (HK-2) were performed to investigate the effect of CRT on high glucose (HG)-induced epithelial-mesenchymal transition (EMT) and the involvement of the PTEN/PI3K/AKT signaling pathway.
UNASSIGNED: CRT treatment significantly improved proteinuria and increased the effective treatment rate in DKD patients compared to the control group, with no significant difference in adverse events. Moreover, CRT reversed HG-induced EMT in HK-2 cells, as evidenced by the downregulation of α-SMA and upregulation of E-cadherin at both mRNA and protein levels. Mechanistically, CRT increased PTEN expression and inhibited the PI3K/AKT pathway, similar to the effects of the PI3K inhibitor LY29400. The combination of CRT and LY29400 further enhanced PTEN mRNA expression under HG conditions.
UNASSIGNED: CRT effectively improves proteinuria in DKD patients and ameliorates HG-induced EMT in HK-2 cells. The underlying mechanism may involve the upregulation of PTEN and subsequent inhibition of the PI3K/AKT signaling pathway. These findings provide new insights into the therapeutic potential of CRT for DKD treatment.
摘要：
■糖尿病肾病（DKD）是糖尿病的严重微血管并发症，可导致终末期肾病。Colquhounia根片（CRT）已显示出治疗DKD的潜力，但其功效和潜在机制仍有待阐明。
■对61例DKD患者进行了一项随机对照临床试验。治疗组除接受标准治疗外还接受CRT,而对照组仅接受标准治疗。治疗3个月后评价疗效和不良反应。此外,使用人肾小管上皮细胞（HK-2）进行了体外实验，以研究CRT对高糖（HG）诱导的上皮间质转化（EMT）的影响以及PTEN/PI3K/AKT信号通路的参与。与对照组相比，
■CRT治疗可明显改善DKD患者的蛋白尿并提高有效治疗率，不良事件无显著差异。此外，CRT逆转HG诱导的HK-2细胞EMT，如在mRNA和蛋白质水平上α-SMA的下调和E-钙黏着蛋白的上调所证明的。机械上,CRT增加PTEN表达并抑制PI3K/AKT通路,与PI3K抑制剂LY29400的效果相似。CRT和LY29400的组合在HG条件下进一步增强PTENmRNA表达。
■CRT可有效改善DKD患者的蛋白尿，并改善HG诱导的HK-2细胞EMT。潜在的机制可能涉及PTEN的上调和随后的PI3K/AKT信号通路的抑制。这些发现为CRT治疗DKD的治疗潜力提供了新的见解。
■对61例DKD患者进行了一项随机对照临床试验。治疗组除接受标准治疗外还接受CRT,而对照组仅接受标准治疗。治疗3个月后评价疗效和不良反应。此外,使用人肾小管上皮细胞（HK-2）进行了体外实验，以研究CRT对高糖（HG）诱导的上皮间质转化（EMT）的影响以及PTEN/PI3K/AKT信号通路的参与。与对照组相比，
■CRT治疗可明显改善DKD患者的蛋白尿并提高有效治疗率，不良事件无显著差异。此外，CRT逆转HG诱导的HK-2细胞EMT，如在mRNA和蛋白质水平上α-SMA的下调和E-钙黏着蛋白的上调所证明的。机械上,CRT增加PTEN表达并抑制PI3K/AKT通路,与PI3K抑制剂LY29400的效果相似。CRT和LY29400的组合在HG条件下进一步增强PTENmRNA表达。
■CRT可有效改善DKD患者的蛋白尿，并改善HG诱导的HK-2细胞EMT。潜在的机制可能涉及PTEN的上调和随后的PI3K/AKT信号通路的抑制。这些发现为CRT治疗DKD的治疗潜力提供了新的见解。
