The Anti-Glioblastoma Effects of Magnolol Are Mediated through Paradoxical Enhancement of Antioxidant Defenses and Induction of Apoptosis
نویسندگان
1 Traditional and Complementary Medicine Research Center, Arak University of Medical Sciences, Arak, Iran
2 Traditional and Complementary Medicine Research Center, Arak University of Medical Sciences, Arak, Iran
3 Traditional and Complementary Medicine Research Center, Arak University of Medical Sciences, Arak, Iran
4 Department of Molecular Medicine and Biotechnology, School of Medicine, Arak University of Medical Sciences, Arak, Iran
doi
10.22074/cellj.2026.2072455.1932چکیده
Objective: We investigated the antitumor effects of magnolol on T98G glioblastoma multiform cells and explored itsunderlying mechanisms, with a focus on oxidative stress modulation.Materials and Methods: In this experimental study, cytotoxicity (MTT assay), proliferation (trypan blue), migration(wound healing), clonogenicity (colony formation), and apoptosis (Hoechst 33342) were assessed. Gene expressionof antioxidant enzymes [superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPX)], apoptotic(BAD, SURVIVIV), cell cycle (CYCLIN D1), and metastatic (MMP-9) markers was evaluated viareverse transcriptionquantitative polymerase chain reaction (RT-qPCR). Antioxidant enzyme activity and total antioxidant capacity (TAC)were measured using commercial kits.Results: Magnolol dose-dependently suppressed cell viability (IC50=72.39 μM), proliferation, migration, and colonyformation. It induced apoptosis, upregulated Bad, SOD, CAT, and GPX expression, and downregulated survivin, cyclinD1, and MMP-9. Crucially, magnolol significantly elevated SOD, CAT, and GPX activities, thereby enhancing totalantioxidant capacityConclusion: Magnolol exerts potent anti-glioblastoma effects by inducing a paradoxical hyper-activation of theantioxidant system, disrupting pro-survival redox signaling, and triggering apoptosis. This novel mechanism highlightsits potential as a therapeutic agent.
