Ferit Anıl KOCABAŞ, Mümin Alper ERDOĞAN, Özlem YILMAZ
Journal of Basic and Clinical Health Sciences - 2026;10(3):481-489
Purpose: Rotenone induces Parkinson's disease-like neurotoxicity through mitochondrial impairment, oxidative stress, and apoptosis. We investigated the neuroprotective efficacy of boldine against rotenone-induced cytotoxicity in human SH-SY5Y neuroblastoma cells. Material and Methods: SH-SY5Y cells were pretreated with boldine (0.1-100 µM) for 2 h before exposure to 200 nM rotenone for 24 h. Cell viability, clonogenic capacity, active caspase-3 levels, and apoptotic nuclear morphology were evaluated using the MTS assay, clonogenic assay, ELISA, and Hoechst 33342 staining, respectively. Results: Rotenone (200 nM) significantly reduced viability to 32.3%, suppressed clonogenic potential (3.9%), and increased active caspase-3 levels (p<0.0001). Pretreatment with 0.1µM boldine markedly restored cell viability to 92.2% and clonogenic activity to 81.9%, while significantly reducing caspase-3 levels and nuclear apoptotic alterations (p<0.0001). Higher boldine concentrations (>=5 muM) exhibited antiproliferative effects. Conclusion: Boldine exhibits a concentration-dependent biphasic response against rotenone-induced neurotoxicity, with marked neuroprotection at low concentrations and antiproliferative effects at higher concentrations. The protective effect of 0.1 µM boldine was associated with attenuation of caspase-3 activation and apoptotic nuclear alterations.
