【摘要】 目的 探究当归芍药散含药血清对高糖诱导HK-2细胞上皮-间充质转化(EMT)的影响机制。方法 制备当归芍药散含药血清，对人肾小管上皮HK-2细胞进行高糖诱导，用CCK-8法筛选最佳血清浓度。实验分为两组：实验1设正常组、高糖组、当归芍药散含药血清组、空白血清对照组；实验2增设AKT激动剂组和PI3K抑制剂组。通过Transwell实验检测细胞迁移能力，RT-qPCR检测Vimentin和E-cadherin的mRNA表达，Western blot检测相关蛋白水平。结果 20%体积分数的DSS显著影响HK-2细胞活力，抑制其迁移。与高糖组相比，当归芍药散含药血清组E-cadherin表达升高，Vimentin表达及p-PI3K/PI3K和p-AKT/AKT比值降低(P<0.05)。实验2加入AKT激动剂和PI3K抑制剂后，进一步验证了当归芍药散通过PI3K/AKT信号通路抑制肾小管上皮细胞间充质转化的过程。结论 当归芍药散通过抑制PI3K/AKT信号通路，有效抑制肾小管上皮细胞转分化。更多还原

【Abstract】 Objective To explore the mechanism by which Danggui Shaoyao San(当归芍药散,DSS) serum inhibits high glucose-induced epithelial-mesenchymal transition(EMT) in HK-2 cells through the PI3K/AKT signaling pathway. Methods DSS serum was prepared and used to induce high glucose in human renal tubular epithelial HK-2 cells. The optimal serum concentration was screened using the CCK-8 assay. There were two experiments. Experiment 1 included the normal group, high glucose group, DSS serum group, and blank serum control group; Experiment 2 was added with an AKT agonist group and a PI3K inhibitor group. In Experiment 1, Transwell assays were performed to detect cell migration ability, RT-qPCR was used to measure mRNA expression of Vimentin and E-cadherin, and Western blot(WB) was used to measure protein levels of relevant markers.Results 20% volume fraction of DSS significantly affected HK-2 cell viability and inhibited migration. Compared with the high glucose group, the DSS serum group showed an increase in E-cadherin expression, and a decrease in Vimentin expression as well as the p-PI3K/PI3K and p-AKT/AKT ratios(P<0.05). In Experiment 2, after the addition of AKT agonist and PI3K inhibitor, it was further confirmed that DSS could inhibit EMT in renal tubular epithelial cells through the PI3K/AKT signaling pathway.Conclusion DSS effectively inhibits EMT of renal tubular epithelial cells by suppressing the PI3K/AKT signaling pathway.更多还原