Ginseng protein improves the subacute Parkinson's model.

Abstract

Objective: 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.

Methods: 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.

Results: 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).

Conclusion: 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.