Momordica Charantia Polysaccharides Attenuates MPP+-Induced Injury in Parkinson's Disease Mice and Cell Models by Regulating TLR4/MyD88/NF-κB Pathway

Objective. To investigate the potential role of Momordica charantia polysaccharides (MCPs) in Parkinson's disease (PD) and reveal the molecular mechanism of its function. Method. 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) and 1-methyl-4-phenylpyridinium (1-methyl-4-phenylpyridinium, MPP+) were used to establish PD mice and cell models. The mice and cells were divided into 4 groups: Control group, Control+MCPs group, PD group, and PD+MCPs group. Pole climbing experiment and Rotarod experiment were used to observe the coordination ability of mice. High-performance liquid chromatography and enzyme-linked immunosorbent assay (ELISA) were used to determine neurotransmitters and metabolites, inflammatory factors TNF-alpha and IL-1 beta, oxidative stress-related markers SOD, MDA, and GSH in striatum tissues. Western blot was used to determine the protein levels of tyrosine hydroxylase (TH), oxidative stress-related protein Cytochrome C (Cytochrome C), and apoptosis-related proteins Bcl-2, Bax, and cleaved Caspase-3 in tissues and cells. Moreover, flow cytometry, PI staining, and fluorescence were used to observe cell apoptosis. Finally, the activation effect of MCPs on TLR4/MyD88/NF-kappa B signaling pathway was observed and verified. Results. Compared with the Control group, MPTP treatment can induce brain damage in mice (all P<0.05), change the metabolic state of neurotransmitters (all P<0.05), induce inflammation (all P<0.05), and induce apoptosis and the occurrence of oxidation reaction (all P<0.05); however, MCPs treatment can significantly reverse the above changes (all P<0.05). In cell models, studies have found that MCPs can play a protective role by regulating the activation state of TLR4/MyD88/NF-kappa B pathway. Conclusion. This study found that the application of MCPs therapy can play anti-inflammatory, antioxidative stress, and antiapoptotic effects in PD by regulating the activation of the TLR4/MyD88/NF-kappa B pathway.