KO-HSIU LUGUANG-YAW LIU2026-10-162026-10-162011-09-01Pure ID: 15178374Pure UUID: cab1787c-8705-4d3c-a47a-2c5fde183ec910.1002/jbt.20391https://www.scopus.com/pages/publications/80053898037https://scholars.csmu.edu.tw/handle/123456789/24360Dibenzoylmethane (DBM) belongs to the flavonoid family and is a minor constituent of the root extract of licorice and the β-diketone analogue of curcumin. It exhibits antimutagenic, anticancer, and chemopreventive effects. Ornithine decarboxylase (ODC), the rate-limiting enzyme of the polyamine biosynthetic pathway, plays an important role in growth, proliferation, and transformation. Our previous studies showed ODC overexpression prevented etoposide-, paclitaxel-, and cisplatin-induced apoptosis. Here, we investigated one mechanism of DBM-induced apoptosis and the antiapoptotic effects of ODC during DBM treatment. We found that DBM induced apoptosis, promoted reactive oxygen species (ROS) generation, and disrupted the mitochondrial membrane potential (Δ ψ m. N-acetylcysteine, a ROS scavenger, reduced DBM-induced apoptosis, which led to the loss of Δ ψ m due to reduced ROS. Overexpression of ODC in parental cells had the same effects as the ROS scavenger. The results demonstrated that DBM-induced apoptosis was a ROS-dependent pathway and ODC overexpression blocked DBM-induced apoptosis by inhibiting intracellular ROS production.8enjournal article