Oenothein B induced human non-small cell lung cancer A549 cell death by ROS-mediated PI3K/Akt/NF-κB signaling pathway.

Oenothein B has a wide range of biological activities. This study assessed the possible mechanism of Oenothein B on lung cancer A549 cell. The results showed that Oenothein B effectively inhibited the proliferation of A549 cells by inducing apoptosis, arrested cell at G1 stage. On the one hand, Oenothein B not only increased the level of intracellular reactive oxygen species (ROS), but induced some apoptotic-related protein expression (cleavage caspase-3, PARP, cytochrome c level in the cytoso, Bax). Moreover, ROS inhibitor and PI3K agonist exhibited significant protection against cell death by Oenothein B. ROS inhibitor significantly abrogated the activation of caspase3/7 and 9 by Oenothein B. On the other hand, the levels of p-Akt and p-Akt, p-NF-κB suppressed by Oenothein B could be offset by treatment with ROS inhibitor. To summarize, these results demonstrated that Oenothein B was able to prevent cell growth by maybe via ROS-mediated PI3K/Akt/NF-κB signaling pathway.