Oenothein B has a wide range of biological activities. The present study probed into the underlying mechanism on how Oenothein B inhibits the proliferation of a lung cancer line A549. Our results showed that Oenothein B effectively inhibited the proliferation of A549 cells by inducing apoptosis and arresting cells at G1 stage. Furthermore, Oenothein B not only increased the level of intracellular reactive oxygen species (ROS), but also induced the upregulation of intracellular apoptotic triggers (cleavage caspase-3, PARP, cytochrome c level in the cytosol, Bax). Moreover, ROS inhibitor (N-acetyl-L-cystein, NAC) and PI3K agonist (Insulin-like growth factor 1, IGF-1) could resist cell proliferation inhibition induced by Oenothein B, respectively. ROS inhibitor significantly abrogated the activation of caspase 3/7 and 9 in the presence of Oenothein B. Additionally, suppression of p-PI3K and p-Akt, p-NF-κB by Oenothein B could be compensated by treatment with ROS inhibitor. To summarize, these results demonstrated that Oenothein B was able to prevent cell proliferation probably via ROS-mediated PI3K/Akt/NF-κB signaling pathway.

皂苷B具有广泛的生物活性。本研究探讨了Oenothein B如何抑制肺癌细胞A549增殖的潜在机制。我们的结果表明，Oenothein B通过诱导细胞凋亡并在G1期阻滞细胞，有效抑制A549细胞的增殖。此外，Oenothein B不仅增加了细胞内活性氧（ROS）的水平，而且还诱导了细胞内凋亡触发因子（裂解caspase-3，PARP，细胞溶胶，Bax中细胞色素c的水平）的上调。此外，ROS抑制剂（N-乙酰基-L-半胱氨酸，NAC）和PI3K激动剂（胰岛素样生长因子1，IGF-1）可以分别抵抗由Oenothein B诱导的细胞增殖抑制。在Oenothein B存在的情况下，ROS抑制剂显着消除了caspase 3/7和9的激活。另外，通过用ROS抑制剂治疗可以补偿Oenothein B对p-PI3K和p-Akt，p-NF-κB的抑制作用。综上所述，这些结果表明，蛇蜡蛋白B可能能够通过ROS介导的PI3K / Akt /NF-κB信号通路阻止细胞增殖。