Dioscin has been known for its anti-cancer activity; however, its detailed molecular mechanisms have not been studied so far. Herein, we evaluated the anti-cancer activity of dioscin for proliferation inhibition and apoptosis in HepG2 cancer cells. Initially, dioscin was purified and identified from Polygonatum sibiricum by HPLC, MS, and NMR analysis, respectively. Dioscin inhibited the cell multiplication at IC₅₀ of 8.34 μM, altered the cell morphology, arrested the cell cycle in G2/M phase and led to considerable programmed cell death. Furthermore, it has efficiently promoted the mitochondrial pathway and death receptor pathway. The inhibition of Caspase-8 and Caspase-9 proteins in these pathways abolished the dioscin induced apoptosis significantly; while dioscin inhibited the PI3K/Akt/mTOR pathway. Moreover, dioscin exposure led to enhanced intracellular ROS generation and the mRNA expression of JNK gene which emphasized their involvement in the apoptosis process in HepG2 cells.

薯os皂素以其抗癌活性而闻名。但是，迄今为止尚未研究其详细的分子机理。本文中，我们评估了薯di皂素对HepG2癌细胞的增殖抑制和凋亡的抗癌活性。最初，通过HPLC，MS和NMR分析纯化并从玉竹中纯化出薯os素。薯os皂甙抑制IC _50时的细胞增殖8.34μM的细胞凋亡，改变了细胞形态，使细胞周期停滞在G2 / M期，并导致了可观的程序性细胞死亡。此外，它有效地促进了线粒体途径和死亡受体途径。Caspase-8和Caspase-9蛋白在这些途径中的抑制作用消除了薯os皂素诱导的细胞凋亡。而薯os皂甙抑制PI3K / Akt / mTOR途径。此外，薯di暴露会增加细胞内ROS的产生和JNK基因的mRNA表达，这表明它们参与了HepG2细胞的凋亡过程。