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+) w...

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Main Authors: Dengjun Guo, Jie Zhou, Meng Zhang, Reyisha Taximaimaiti, Xiaoping Wang, Hai Wang
Format: Article
Language:English
Published: Wiley 2021-01-01
Series:International Journal of Polymer Science
Online Access:http://dx.doi.org/10.1155/2021/5575636
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author Dengjun Guo
Jie Zhou
Meng Zhang
Reyisha Taximaimaiti
Xiaoping Wang
Hai Wang
author_facet Dengjun Guo
Jie Zhou
Meng Zhang
Reyisha Taximaimaiti
Xiaoping Wang
Hai Wang
author_sort Dengjun Guo
collection DOAJ
description 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-α and IL-1β, 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-κB 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-κB 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-κB pathway.
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series International Journal of Polymer Science
spelling doaj-art-c5b79c6c491741d3bbc30a07fef147712025-02-03T05:57:51ZengWileyInternational Journal of Polymer Science1687-94221687-94302021-01-01202110.1155/2021/55756365575636Momordica Charantia Polysaccharides Attenuates MPP+-Induced Injury in Parkinson’s Disease Mice and Cell Models by Regulating TLR4/MyD88/NF-κB PathwayDengjun Guo0Jie Zhou1Meng Zhang2Reyisha Taximaimaiti3Xiaoping Wang4Hai Wang5Department of Neurology, Tongde Hospital of Zhejiang Province, Hangzhou, Zhejiang Province 310012, ChinaCenter for Medicinal Resources Research, Zhejiang Academy of Traditional Chinese Medicine, Hangzhou, Zhejiang Province 310012, ChinaDepartment of Clinical Laboratory, Tongde Hospital of Zhejiang Province, Hangzhou, Zhejiang Province 310012, ChinaDepartment of Neurology, Tongren Hospital, Shanghai Jiao Tong University Medical School, Shanghai 200336, ChinaDepartment of Neurology, Tongren Hospital, Shanghai Jiao Tong University Medical School, Shanghai 200336, ChinaDepartment of Clinical Laboratory, Tongde Hospital of Zhejiang Province, Hangzhou, Zhejiang Province 310012, ChinaObjective. 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-α and IL-1β, 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-κB 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-κB 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-κB pathway.http://dx.doi.org/10.1155/2021/5575636
spellingShingle Dengjun Guo
Jie Zhou
Meng Zhang
Reyisha Taximaimaiti
Xiaoping Wang
Hai Wang
Momordica Charantia Polysaccharides Attenuates MPP+-Induced Injury in Parkinson’s Disease Mice and Cell Models by Regulating TLR4/MyD88/NF-κB Pathway
International Journal of Polymer Science
title Momordica Charantia Polysaccharides Attenuates MPP+-Induced Injury in Parkinson’s Disease Mice and Cell Models by Regulating TLR4/MyD88/NF-κB Pathway
title_full Momordica Charantia Polysaccharides Attenuates MPP+-Induced Injury in Parkinson’s Disease Mice and Cell Models by Regulating TLR4/MyD88/NF-κB Pathway
title_fullStr Momordica Charantia Polysaccharides Attenuates MPP+-Induced Injury in Parkinson’s Disease Mice and Cell Models by Regulating TLR4/MyD88/NF-κB Pathway
title_full_unstemmed Momordica Charantia Polysaccharides Attenuates MPP+-Induced Injury in Parkinson’s Disease Mice and Cell Models by Regulating TLR4/MyD88/NF-κB Pathway
title_short Momordica Charantia Polysaccharides Attenuates MPP+-Induced Injury in Parkinson’s Disease Mice and Cell Models by Regulating TLR4/MyD88/NF-κB Pathway
title_sort momordica charantia polysaccharides attenuates mpp induced injury in parkinson s disease mice and cell models by regulating tlr4 myd88 nf κb pathway
url http://dx.doi.org/10.1155/2021/5575636
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