Ginseng protein improves the subacute Parkinson's model

To investigate the ameliorative effect of total ginseng protein (GP) on Parkinson's disease (PD) in vivo and in vitro and its effect on the intestinal flora.

In the in vitro studies, PC12 cells were treated with 1 mM 1-methyl-4-phenyl-pyridinium ion (MPP+), and C57BL/6 mice were injected intraperitoneally with 1-methyl-4-phenyl-1, 2, 3, 6-tetrahydropyridine (MPTP) at a concentration of 35 mg∙kg^-1. Cell activity, behavioral, brain histopathology, and intestinal flora analyses were performed to investigate the ameliorative effects of long-term feeding of low, medium, and high doses of GP on the MPTP-induced subacute PD model in C57BL/6 mice.

In vitro, GP (20-100 μg·mL^{- 1}) showed no toxicity to PC12 cells. MPP⁺ (1.0 mM, 12 h) reduced cell viability to 71.9% (^##p < 0.01), while GP treatment (24 h) reversed MPP⁺ -induced apoptosis, elevating survival rates by 14.4-29.3% (^***p < 0.001). Behavioral tests in subacute PD mice revealed medium-dose GP (GPM) significantly improved rod-climbing duration and rotarod latency (^*p < 0.05). Antioxidant assays showed GPM enhanced total antioxidant capacity and SOD activity (^*p < 0.05) while reducing lipid oxidation. Histopathological analysis indicated GP restored hippocampal CA1 neuron integrity and upregulated tyrosine hydroxylase (TH) expression (^***p < 0.001) while suppressing α-synuclein (α-Syn) (^**p < 0.01~^***p < 0.001). Intestinal flora analysis demonstrated GP modulated microbial diversity (Chao1/Shannon indices), with GPM shifting community structure closer to controls (PCoA).

GP has an ameliorative effect on MPP±injured PC12 cells and improves behavioral disorders, brain and intestinal histopathological injuries, and intestinal flora disorders in subacute PD model C57BL/6 mice.