Glycitein exerts neuroprotective effects in Rotenone-triggered oxidative stress and apoptotic cell death in the cellular model of Parkinson’s disease

Abstract

Parkinson’s disease (PD) is one of the prevalent neurodegenerative diseases among aging populations. Despite recent advancements, still, no therapy exists for the prevention of PD. Given the remarkable pharmacological properties of flavonoids, this study was designed to investigate the protective effects of a plant-derived flavonoid, glycitein in a cellular model of PD. Rotenone, a prevalently used pesticide, has been employed to study the pathology of PD. The results of the present study showed that Glycitein significantly (P<0.05) prevented the rotenone-induced inhibition of cell viability as evident from the MTT assay. Additionally, it was found that the increased ROS levels triggered by rotenone in human SK-N-SH neuroblastoma cells were significantly (P<0.05) diminished upon glycitein treatment. Glycitein treatment also restored the mitochondrial membrane potential of the rotenone treated SK-N-SH cells. These effects of Glycitein were mainly due to its ability to trigger the increased activity of the ROS scavenging enzymes such as GSH, SOD and CAT. The ATP estimates showed that the ATP levels were significantly (P<0.05) reduced in the rotenone treated SK-N-SH cells. Nonetheless, glycitein treatment could restore the ATP levels of the SK-N-SH cells in a dose-dependent manner. Rotenone has also been shown to induce apoptosis in human cells and the results of the annexin V/PI staining showed that glycitein exhibits remarkable potential to prevent in the rotenone triggered apoptosis in SK-N-SH cells. This was also accompanied by alteration in the expression of Bax, Bcl-2 and caspase-3 expression. Taken together, the study indicates that glycitein exhibits neuroprotective effects by preventing rotenone induce oxidative stress and apoptotic cell death. These findings point towards the use of glycitein in the management of neurodegenerative diseases such as PD.