Abstract

Background: Parkinson’s disease (PD) is regarded as a neurological condition in which continuous degeneration of dopaminergic neurons occurs selectively. Currently, most treatments for neurodegenerative diseases are palliative. According to in vitro and in vivo models of PD in recent studies, hesperidin (Hsd) showed protective properties during neuron damage. Moreover, recent reports demonstrated the induction of Hsd. Aims and Objectives: The current study aimed at analyzing the protective effect of Hsd, as a major flavanone constituent by determining its effect on 6-hydroxydopamine (OHDA)-mediated oxidative stress. The current study analyzed the impact of Hsd on neurotoxicity, mediated by 6-OHDA, in SH-SY5Y cells by an in vitro model of PD.
Materials and Methods: The study employed 150 μM of 6-OHDA to induce cellular damage. Furthermore, 3-(4,5-dimethylthiazol-2-Yl)-2,5-diphenyltetrazolium bromide test was performed to analyze cellular viability. Fluorescence spectrophotometry was performed to measure the level of intracellular reactive oxygen species (ROS) and intracellular calcium. Based on the findings, 6-OHDA could reduce cell viability.
Results: Moreover, intracellular ROS, intracellular calcium, and DNA fragmentation vastly improved in cells exposed to 6-OHDA. SH-SY5Y cell incubation with Hsd (1 and 10 μg/mL)-induced protective effects and decreased the biochemical markers of cell apoptosis. According to the findings, Hsd showed protective features against neurotoxicity, caused by 6-OHDA. These protective properties were accompanied by anti-apoptotic features. Conclusion: It was revealed that Hsd affected the management of PD. Given the preserved mitochondrial function of Hsd , and its antioxidant and anti-apoptotic properties in neuroblastoma cell lines, this compound has neuroprotective effects on 6-OHDA.