Protective role of Ocimum sanctum leaf extracts against rotenone induced cytotoxicity and oxidative stress in SH-SY5Y neuroblastoma cell line.

Ocimum sanctum (OS) encompasses a spectrum of bioactive secondary metabolites, including flavonoids and phenolic compounds, which have demonstrated potential therapeutic effects in neurological and cardiovascular disorders. The present investigation explored the neuroprotective ability of methanolic (OSM) and ethanolic (OSE) extracts of OS leaves against rotenone-induced cytotoxicity and oxidative stress in SH-SY5Y human neuroblastoma cells, an established in vitro model of Parkinson's disease (PD). Cells were pre-treated with OSM or OSE (100 μg/mL) extracts prior to rotenone exposure, and neuroprotective efficacy was evaluated. Results showed that rotenone significantly reduced cell viability, increased intracellular and mitochondrial reactive oxygen species (ROS) generation, disrupted mitochondrial membrane potential, decreased the expression of PD-associated marker proteins (Parkin, DJ-1, BDNF, and tyrosine hydroxylase) and promoted α-synuclein aggregation. Pre-treatment with both OSM and OSE extracts significantly attenuated these pathological changes, with OSE extract consistently exhibiting greater neuroprotective efficacy than OSM extract. The findings demonstrate that OS, particularly its OSE extract, protects neuronal cells by reducing oxidative stress, preserving mitochondrial function, restoring PD-associated protein expression, and suppressing α-synuclein aggregation. These results highlight the therapeutic potential of OS as a promising neuroprotective candidate for mitigating mitochondrial dysfunction associated with PD.