The anti-glioblastoma effects of magnolol are mediated through paradoxical enhancement of antioxidant defenses and induction of apoptosis.
The Anti-Glioblastoma Effects of Magnolol Are Mediated through Paradoxical Enhancement of Antioxidant Defenses and Induction of Apoptosis.
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Abstract
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: In this experimental study, cytotoxicity (MTT assay), proliferation (trypan blue), migration (wound healing), clonogenicity (colony formation), and apoptosis (Hoechst 33342) were assessed. Gene expression of antioxidant enzymes [superoxide dismutase (), catalase (), glutathione peroxidase ()], apoptotic (), cell cycle (), and metastatic () 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: Magnolol dose-dependently suppressed cell viability (IC=72.39μM), 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.
Affiliation
Mohammad Zand
External References
- PubMed ID:
- 42051074
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