Randomized trial investigates magnolol's impact on glioblastoma, revealing mechanisms for therapeutic potential.
Objective: We investigated the antitumor effects of magnolol on T98G glioblastoma multiform cells and explored its underlying mechanisms, with a focus on oxidative stress modulation. Materials and Methods: ) markers was evaluated viareverse transcription quantitative polymerase chain reaction (RT-qPCR). Antioxidant enzyme activity and total antioxidant capacity (TAC) were measured using commercial kits. Results: =72.39 μM), proliferation, migration, and colony formation. It induced apoptosis, upregulated Bad, SOD, CAT, and GPX expression, and downregulated survivin, cyclin D1, and MMP-9. Crucially, magnolol significantly elevated SOD, CAT, and GPX activities, thereby enhancing total antioxidant capacity. Conclusion: Magnolol exerts potent anti-glioblastoma effects by inducing a paradoxical hyper-activation of the antioxidant system, disrupting pro-survival redox signaling, and triggering apoptosis. This novel mechanism highlights its potential as a therapeutic agent.
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Zand et al. (2026) studied this question.
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