PDF(Pubmed)
Abstract：
The aim of this research was to discuss Hederagenin\'s antitumor effects on glioma by in vitro study. U251 and U87 cell lines were used as research target in our research. In the first step, the different Hed concentrations were treated to U251 and U87 cell lines, and the second step is Nur77 transfection in U251 and U87 with Hed treatment; measuring cell proliferation by MTT and EdU staining; evaluating cell invasion and migration abilities by transwell assay and relative gene and protein expressions by RT-qPCR and WB assay. Compared with NC group, U251 and U87 cell proliferation were significantly depressed with cell apoptosis significantly increasing, and cell invasion and migration abilities were significantly inhibited in Hed-treated groups (p < .05, respectively); however, with Nur77 transfection, the Hed\'s antitumor effects disappeared. Meanwhile, with Hed supplement, Nur77, PI3K, and AKT gene expressions were significantly downregulated (p < .05, respectively) in Hed-treated groups; and Nur77, p-PI3K, and p-AKT protein expressions were significantly decreased (p < .05, respectively) in Hed-treated groups. Hed had antitumor effects on glioma cell biological activities via Nur77/PI3K/AKT pathway in vitro study.
摘要：
本研究旨在通过体外研究探讨Hederagenin对胶质瘤的抗肿瘤作用。U251和U87细胞系在我们的研究中被用作研究目标。第一步,将不同的Hed浓度处理到U251和U87细胞系中，第二步是用Hed处理在U251和U87中转染Nur77；通过MTT和EdU染色测量细胞增殖；通过transwell测定评估细胞的侵袭和迁移能力，通过RT-qPCR和WB测定评估相对基因和蛋白质的表达。与NC组相比,U251和U87细胞增殖显著抑制，细胞凋亡显著增加，Hed处理组的细胞侵袭和迁移能力受到显著抑制(分别为p<0.05);用Nur77转染，Hed的抗肿瘤作用消失了.同时,用Hed补充剂，Nur77,PI3K,和AKT基因表达在Hed治疗组中显著下调(分别为p<0.05)；和Nur77，p-PI3K，和p-AKT蛋白表达在Hed治疗组中显著降低(分别为p<0.05)。在体外研讨中，Hed经由过程Nur77/PI3K/AKT通路对胶质瘤细胞生物学活性具有抗肿瘤感化。
