Integrated phytochemical profiling and molecular modelling of Magnolia officinalis bark-derived bioactive compounds interacting with apoptosis-associated proteins relevant to cisplatin-induced cellular injury

Introduction Cisplatin is an effective chemotherapeutic agent; however, oxidative stress and apoptosis-associated signalling contribute to both its therapeutic effects and dose-limiting toxicities. This study investigated the phytochemical composition and antioxidant properties of Magnolia officinalis bark extract and explored the predicted interactions of selected constituents with the apoptosis-associated proteins caspase-3 and BCL-2. Methods Phenolic and flavonoid contents, DPPH and ABTS radical-scavenging activities, chromatographic–mass spectrometric profiling, molecular docking, pharmacokinetic and toxicity predictions, 100-ns molecular dynamics simulations, and MM/GBSA calculations were employed. Results Among the solvent extracts evaluated, the methanolic extract exhibited the highest phenolic (64.55 ± 0.65 mg GAE/g dry extract) and flavonoid (21.90 ± 0.55 mg QE/g dry extract) contents. It also demonstrated concentration-dependent DPPH and ABTS radical-scavenging activities, with IC₅₀ values of 143.02 and 326.01 µg/mL, respectively. Phytochemical profiling provided tentative evidence for multiple constituents, with magnolol and honokiol prioritised for computational evaluation. Molecular docking and dynamics analyses indicated predicted protein–ligand interactions and complex-specific conformational behaviour, including substantial magnolol displacement or rearrangement in the caspase-3 system during approximately 45–65 ns. Discussion The findings provide insights into the antioxidant and phytochemical properties of Magnolia officinalis bark extract and identify candidate constituents for further investigation. However, the computational results are hypothesis-generating and do not establish functional modulation of caspase-3 or BCL-2. Because cisplatin exposure and target-specific activity were not experimentally evaluated, conclusions regarding cytoprotection, chemosensitisation, or target activation/inhibition cannot be drawn. Further validation using target-specific biochemical assays and cisplatin-exposed cellular models is warranted.