Sodium Butyrate Exacerbates Parkinson’s Disease by Aggravating Neuroinflammation and Colonic Inflammation in MPTP-Induced Mice Model

The abnormal production of short chain fatty acid (SCFAs) caused by gut microbial dysbiosis plays an important role in the pathogenesis and progression of Parkinson’s disease (PD). This study sought to evaluate how butyrate, one of SCFAs, affect the pathology in a subacute 1-methyl-4-phenyl-1,2,3,6-...

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Published inNeurochemical research Vol. 45; no. 9; pp. 2128 - 2142
Main Authors Qiao, Chen-Meng, Sun, Meng-Fei, Jia, Xue-Bing, Li, Yang, Zhang, Bo-Ping, Zhao, Li-Ping, Shi, Yun, Zhou, Zhi-Lan, Zhu, Ying-Li, Cui, Chun, Shen, Yan-Qin
Format Journal Article
LanguageEnglish
Published New York Springer US 01.09.2020
Springer Nature B.V
Subjects
Astrocytes
Biochemistry
Biomedical and Life Sciences
Biomedicine
Cell Biology
Colon
Cytokines
Dopamine
Dopamine receptors
Dysbacteriosis
Fatty acids
Hydroxylase
IL-1β
Inflammation
Interleukin 18
Interleukin 6
Intestinal microflora
Lipopolysaccharides
Microglia
Microorganisms
Movement disorders
MPTP
MyD88 protein
Neurochemistry
Neurodegenerative diseases
Neurology
Neuronal-glial interactions
Neurosciences
NF-κB protein
Nitric-oxide synthase
Original Paper
Parkinson's disease
Pathogenesis
Signal transduction
Sodium
Sodium butyrate
Tumor necrosis factor-α
Tyrosine
Tyrosine 3-monooxygenase
Sodium butyrate
Parkinson’s disease (PD)
Neuroinflammation
MPTP
Colonic inflammation
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Abstract The abnormal production of short chain fatty acid (SCFAs) caused by gut microbial dysbiosis plays an important role in the pathogenesis and progression of Parkinson’s disease (PD). This study sought to evaluate how butyrate, one of SCFAs, affect the pathology in a subacute 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine hydrochloride (MPTP) treated mouse model of PD. Sodium butyrate (NaB; 165 mg/kg/day i.g . , 7 days) was administrated from the day after the last MPTP injection. Interestingly, NaB significantly aggravated MPTP-induced motor dysfunction ( P  < 0.01), decreased dopamine ( P  < 0.05) and 5-HT ( P  < 0.05) levels, exacerbated declines of dopaminergic neurons (34%, P  < 0.05) and downregulated expression of tyrosine hydroxylase (TH, 47%, P  < 0.05), potentiated glia-mediated neuroinflammation by increasing the number of microglia (17%, P  < 0.05) and activating astrocytes (28%, P  < 0.01). In vitro study also confirmed that NaB could significantly exacerbate pro-inflammatory cytokines expression (IL-1β, 4.11-fold, P  < 0.01; IL-18, 3.42-fold, P  < 0.01 and iNOS, 2.52-fold, P  < 0.05) and NO production (1.55-fold, P  < 0.001) in LPS-stimulated BV2 cells. In addition, NaB upregulated the expression of pro-inflammatory cytokines (IL-6, 3.52-fold, P  < 0.05; IL-18, 1.72-fold, P  < 0.001) and NLRP3 (3.11-fold, P  < 0.001) in the colon of PD mice. However, NaB had no effect on NFκB, MyD88 and TNF-α expression in PD mice. Our results indicate that NaB exacerbates MPTP-induced PD by aggravating neuroinflammation and colonic inflammation independently of the NFκB/MyD88/TNF-α signaling pathway.
AbstractList The abnormal production of short chain fatty acid (SCFAs) caused by gut microbial dysbiosis plays an important role in the pathogenesis and progression of Parkinson’s disease (PD). This study sought to evaluate how butyrate, one of SCFAs, affect the pathology in a subacute 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine hydrochloride (MPTP) treated mouse model of PD. Sodium butyrate (NaB; 165 mg/kg/day i.g . , 7 days) was administrated from the day after the last MPTP injection. Interestingly, NaB significantly aggravated MPTP-induced motor dysfunction ( P  < 0.01), decreased dopamine ( P  < 0.05) and 5-HT ( P  < 0.05) levels, exacerbated declines of dopaminergic neurons (34%, P  < 0.05) and downregulated expression of tyrosine hydroxylase (TH, 47%, P  < 0.05), potentiated glia-mediated neuroinflammation by increasing the number of microglia (17%, P  < 0.05) and activating astrocytes (28%, P  < 0.01). In vitro study also confirmed that NaB could significantly exacerbate pro-inflammatory cytokines expression (IL-1β, 4.11-fold, P  < 0.01; IL-18, 3.42-fold, P  < 0.01 and iNOS, 2.52-fold, P  < 0.05) and NO production (1.55-fold, P  < 0.001) in LPS-stimulated BV2 cells. In addition, NaB upregulated the expression of pro-inflammatory cytokines (IL-6, 3.52-fold, P  < 0.05; IL-18, 1.72-fold, P  < 0.001) and NLRP3 (3.11-fold, P  < 0.001) in the colon of PD mice. However, NaB had no effect on NFκB, MyD88 and TNF-α expression in PD mice. Our results indicate that NaB exacerbates MPTP-induced PD by aggravating neuroinflammation and colonic inflammation independently of the NFκB/MyD88/TNF-α signaling pathway.
The abnormal production of short chain fatty acid (SCFAs) caused by gut microbial dysbiosis plays an important role in the pathogenesis and progression of Parkinson’s disease (PD). This study sought to evaluate how butyrate, one of SCFAs, affect the pathology in a subacute 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine hydrochloride (MPTP) treated mouse model of PD. Sodium butyrate (NaB; 165 mg/kg/day i.g., 7 days) was administrated from the day after the last MPTP injection. Interestingly, NaB significantly aggravated MPTP-induced motor dysfunction (P < 0.01), decreased dopamine (P < 0.05) and 5-HT (P < 0.05) levels, exacerbated declines of dopaminergic neurons (34%, P < 0.05) and downregulated expression of tyrosine hydroxylase (TH, 47%, P < 0.05), potentiated glia-mediated neuroinflammation by increasing the number of microglia (17%, P < 0.05) and activating astrocytes (28%, P < 0.01). In vitro study also confirmed that NaB could significantly exacerbate pro-inflammatory cytokines expression (IL-1β, 4.11-fold, P < 0.01; IL-18, 3.42-fold, P < 0.01 and iNOS, 2.52-fold, P < 0.05) and NO production (1.55-fold, P < 0.001) in LPS-stimulated BV2 cells. In addition, NaB upregulated the expression of pro-inflammatory cytokines (IL-6, 3.52-fold, P < 0.05; IL-18, 1.72-fold, P < 0.001) and NLRP3 (3.11-fold, P < 0.001) in the colon of PD mice. However, NaB had no effect on NFκB, MyD88 and TNF-α expression in PD mice. Our results indicate that NaB exacerbates MPTP-induced PD by aggravating neuroinflammation and colonic inflammation independently of the NFκB/MyD88/TNF-α signaling pathway.
The abnormal production of short chain fatty acid (SCFAs) caused by gut microbial dysbiosis plays an important role in the pathogenesis and progression of Parkinson's disease (PD). This study sought to evaluate how butyrate, one of SCFAs, affect the pathology in a subacute 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine hydrochloride (MPTP) treated mouse model of PD. Sodium butyrate (NaB; 165 mg/kg/day i.g., 7 days) was administrated from the day after the last MPTP injection. Interestingly, NaB significantly aggravated MPTP-induced motor dysfunction (P < 0.01), decreased dopamine (P < 0.05) and 5-HT (P < 0.05) levels, exacerbated declines of dopaminergic neurons (34%, P < 0.05) and downregulated expression of tyrosine hydroxylase (TH, 47%, P < 0.05), potentiated glia-mediated neuroinflammation by increasing the number of microglia (17%, P < 0.05) and activating astrocytes (28%, P < 0.01). In vitro study also confirmed that NaB could significantly exacerbate pro-inflammatory cytokines expression (IL-1β, 4.11-fold, P < 0.01; IL-18, 3.42-fold, P < 0.01 and iNOS, 2.52-fold, P < 0.05) and NO production (1.55-fold, P < 0.001) in LPS-stimulated BV2 cells. In addition, NaB upregulated the expression of pro-inflammatory cytokines (IL-6, 3.52-fold, P < 0.05; IL-18, 1.72-fold, P < 0.001) and NLRP3 (3.11-fold, P < 0.001) in the colon of PD mice. However, NaB had no effect on NFκB, MyD88 and TNF-α expression in PD mice. Our results indicate that NaB exacerbates MPTP-induced PD by aggravating neuroinflammation and colonic inflammation independently of the NFκB/MyD88/TNF-α signaling pathway.The abnormal production of short chain fatty acid (SCFAs) caused by gut microbial dysbiosis plays an important role in the pathogenesis and progression of Parkinson's disease (PD). This study sought to evaluate how butyrate, one of SCFAs, affect the pathology in a subacute 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine hydrochloride (MPTP) treated mouse model of PD. Sodium butyrate (NaB; 165 mg/kg/day i.g., 7 days) was administrated from the day after the last MPTP injection. Interestingly, NaB significantly aggravated MPTP-induced motor dysfunction (P < 0.01), decreased dopamine (P < 0.05) and 5-HT (P < 0.05) levels, exacerbated declines of dopaminergic neurons (34%, P < 0.05) and downregulated expression of tyrosine hydroxylase (TH, 47%, P < 0.05), potentiated glia-mediated neuroinflammation by increasing the number of microglia (17%, P < 0.05) and activating astrocytes (28%, P < 0.01). In vitro study also confirmed that NaB could significantly exacerbate pro-inflammatory cytokines expression (IL-1β, 4.11-fold, P < 0.01; IL-18, 3.42-fold, P < 0.01 and iNOS, 2.52-fold, P < 0.05) and NO production (1.55-fold, P < 0.001) in LPS-stimulated BV2 cells. In addition, NaB upregulated the expression of pro-inflammatory cytokines (IL-6, 3.52-fold, P < 0.05; IL-18, 1.72-fold, P < 0.001) and NLRP3 (3.11-fold, P < 0.001) in the colon of PD mice. However, NaB had no effect on NFκB, MyD88 and TNF-α expression in PD mice. Our results indicate that NaB exacerbates MPTP-induced PD by aggravating neuroinflammation and colonic inflammation independently of the NFκB/MyD88/TNF-α signaling pathway.
Author Zhang, Bo-Ping
Cui, Chun
Shen, Yan-Qin
Zhao, Li-Ping
Shi, Yun
Li, Yang
Zhou, Zhi-Lan
Sun, Meng-Fei
Zhu, Ying-Li
Jia, Xue-Bing
Qiao, Chen-Meng
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  organization: Public Health Research Center at Jiangnan University, Wuxi School of Medicine, Jiangnan University
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IngestDate Fri Jul 11 10:09:26 EDT 2025
Sat Aug 16 15:22:44 EDT 2025
Thu Apr 24 23:07:25 EDT 2025
Tue Jul 01 03:43:15 EDT 2025
Fri Feb 21 02:32:11 EST 2025
IsPeerReviewed true
IsScholarly true
Issue 9
Keywords Sodium butyrate
Parkinson’s disease (PD)
Neuroinflammation
MPTP
Colonic inflammation
Language English
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crossref_citationtrail_10_1007_s11064_020_03074_3
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  year: 2020
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PublicationTitle Neurochemical research
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Snippet The abnormal production of short chain fatty acid (SCFAs) caused by gut microbial dysbiosis plays an important role in the pathogenesis and progression of...
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SubjectTerms Astrocytes
Biochemistry
Biomedical and Life Sciences
Biomedicine
Cell Biology
Colon
Cytokines
Dopamine
Dopamine receptors
Dysbacteriosis
Fatty acids
Hydroxylase
IL-1β
Inflammation
Interleukin 18
Interleukin 6
Intestinal microflora
Lipopolysaccharides
Microglia
Microorganisms
Movement disorders
MPTP
MyD88 protein
Neurochemistry
Neurodegenerative diseases
Neurology
Neuronal-glial interactions
Neurosciences
NF-κB protein
Nitric-oxide synthase
Original Paper
Parkinson's disease
Pathogenesis
Signal transduction
Sodium
Sodium butyrate
Tumor necrosis factor-α
Tyrosine
Tyrosine 3-monooxygenase
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Title Sodium Butyrate Exacerbates Parkinson’s Disease by Aggravating Neuroinflammation and Colonic Inflammation in MPTP-Induced Mice Model
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