Mitochondria-mediated apoptotic induction byMitochondria-mediated apoptotic induction by Chionanthus Chionanthus virginica virginica Q: A cytotoxic and oxidative stress-driven approach in Q

Abstract

Background: Hepatocellular carcinoma (HCC) is a leading cause of cancer-related deaths worldwide, with current therapeutic options limited by late-stage detection, recurrence, and toxicity. Alternative treatments derived from medic-inal plants are gaining attention due to their potential anticancer properties. Chionanthus virginica, traditionally used for liver disorders, contains bioactive compounds with hepatoprotective and antioxidant effects. However, its anticancer potential remains largely unexplored. Objective: This study evaluates the antioxidant, cytotoxic, and apoptotic effects of Chionanthus virginica in mother tincture (Q) and potentised (12C) forms on HepG2 liver cancer cells to determine its efficacy as a natural anticancer agent. Materials and methods: HepG2 cells were treated with Chionanthus virginica Q and 12C across defined exposure levels (50–1000 μL/mL; extract-equivalent for Q and volume-equivalent for 12C). Antioxidant activity was determined using the DPPH assay, while MTT and LDH assays assessed cytotoxicity. Mitochondrial dysfunction was analysed via MMP and cytochrome c release assays, ROS generation was measured by DCFH-DA fluorescence, and caspase activity was quantified using a colorimetric assay. Results: Chionanthus virginica Q showed the strongest antioxidant activity (IC50 = 101.49 μg/mL) and higher cytotoxicity (CTC50 = 330.35 μg/mL), while the response observed with Chionanthus virginica 12C was interpreted only as a biological effect under volume-equivalent exposure conditions. One-way and two-way ANOVA were performed for statistical significance. LDH release, cytochromec translocation, and ROS levels increased significantly (p < 0.001), leading to mitochondrial depolarisation and caspase activation, confirming apoptosis. Conclusion: This study demonstrates that Chionanthus virginica Q induces apoptosis in HepG2 cells via oxidative stress and mitochondrial dysfunction, supporting its potential as a natural anticancer agent. Further studies should focus on bioactive compound isolation and in vivo validation.