Cortex Periplocae (CP) 的活性成分在许多癌症中发挥抗肿瘤特性。然而，人们对它们对神经胶质瘤的影响或相关的潜在机制知之甚少。该研究调查了CP治疗神经胶质瘤的潜在机制。用CP的乙醇提取物处理U251和TG905细胞。使用细胞计数试剂盒-8 (CCK-8) 和集落形成测定检测细胞增殖。应用流式细胞术分析来探索细胞周期停滞和细胞凋亡的诱导。 Western blot检测细胞周期和凋亡相关蛋白的表达水平。采用网络药理学方法预测 CP 活性成分对神经胶质瘤作用的潜在机制。然后，使用基于相对和绝对定量的同量异位标签（iTRAQ）的定量蛋白质组学分析来验证差异表达的蛋白质和通路，以揭示潜在的机制。此外，为了确定 iTRAQ 结果，使用平行反应监测 (PRM) 选择 6 种候选蛋白进行定量。CP 提取物抑制 U251 和 TG905 细胞的增殖并诱导细胞周期停滞和凋亡。 CP有16种活性化合物。 CP的抗肿瘤机制可能与细胞凋亡通路、p53信号通路、PI3K-AKT通路或癌症通路中的转录失调有关。六种蛋白（HSP90AB1、TOP2A、ATP1A1、TGFβ1、ATP1B1 和 TYMS）被确定为调节胶质瘤 CP 的关键因子。我们的研究利用集成网络药理学和基于 iTRAQ 的定量蛋白质组学揭示了 CP 治疗胶质瘤的潜在机制技术。

The active components of Cortex Periplocae (CP) exert antitumor properties in many cancers. However, little is known about their effects on glioma or the related underlying mechanisms.The study investigated the underlying mechanism of CP in treating glioma.The U251 and TG905 cells were treated with an ethanol extract from CP. Cell proliferation was detected using Cell Counting Kit-8 (CCK-8) and a colony formation assay. The flow cytometric analysis was applied to explore the induction of cell cycle arrest and apoptosis. The expression levels of cell cycleand apoptosis-associated proteins were measured with western blot. A network pharmacology method was performed to predict the potential mechanism underlying the effects of the active components of CP on glioma. Then, isobaric tags for relative and absolute quantitation (iTRAQ)-based quantitative proteomics analysis was used to verify the differentially expressed proteins and pathways in order to reveal the underlying mechanisms. Furthermore, to determine the iTRAQ results, 6 candidate proteins were chosen for quantification using parallel reaction monitoring (PRM).The CP extract inhibited the proliferation of U251 and TG905 cells and induced cell cycle arrest and apoptosis. There are 16 active compounds of CP. The antitumor mechanism of CP may be related to the apoptosis pathway, p53 signaling pathway, PI3K-AKT pathway, or transcriptional misregulation in cancer pathway. Six proteins (HSP90AB1, TOP2A, ATP1A1, TGFβ1, ATP1B1, and TYMS) were determined to be key factors involved in regulating CP in glioma.Our research revealed the underlying mechanism of CP in treating glioma using integrated network pharmacology and iTRAQ-based quantitative proteomics technology.