Sorghum bicolor supplement attenuates rotenone-induced behavioral derangements in rats through neuroprotective mechanisms and modulation of tyrosine hydroxylase and α-synuclein/NF-kB immunopositive cells expressions.

The loss of dopamine due to progressive degeneration of dopaminergic neurons is the primary cause of neurobehavioral disturbances in Parkinson's disease (PD). Current research focuses on developing neuroprotective agents that can halt the progressive degeneration of dopaminergic neurons in PD, as its cure remains elusive. Several herbal products, including extracts from Sorghum bicolor, which possess neuroprotective properties, are being investigated as potential agents for PD. In this study, we investigated the effects of Sorghum bicolor supplement (SbS) on rotenone-induced neurobehavioral and neuropathological derangements in male Wistar rats. The rats were distributed into six groups (n = 7): group 1 received vehicle (control), group 2 also received vehicle (rotenone-control), group 3-5 had SbS (50, 100 and 200 mg/kg) while group 6 received Levodopa-carbidopa (10 mg/kg), orally for 28 days. In addition, group 2-6 also received intraperitoneal injections of rotenone (2.5 mg/kg), 30 min after each treatment, on alternate days for 28 days. Neurobehavioral functions were evaluated on day 28 using a hanging wire test for motor function, Y-maze for memory, and sucrose splash test for depression. The rats' brain contents of myeloperoxidase, acetylcholinesterase, dopamine, tyrosine hydroxylase (TH), caspase-3, nuclear factor kappa B (NF-κB), and α-synuclein were determined. Histomorphological changes and dendritic arborizations were assessed. The SbS attenuates motor deficit, memory dysfunction, and depression-like effects in rotenone-treated rats. The supplement modulates myeloperoxidase, acetylcholinesterase, caspase-3, TH, NF-κB, and α-synuclein contents in rotenone-treated rats. Rotenone-induced histomorphological alterations, loss of neuronal cell viability, and dendritic arbors were abrogated by SbS. The findings suggest that SbS attenuates rotenone-induced behavioral deficits in rats through neuroprotective mechanisms and modulation of TH and α-synuclein/NF-kB immunopositive cell expressions.