MPTP-Induced Neuroinflammation Increases the Expression of Pro-Inflammatory Cytokines and Their Receptors in Mouse Brain

被引：88

作者：

Lofrumento, Dario Domenico ^{[2
]}

Saponaro, Concetta ^{[1
]}

Cianciulli, Antonia ^{[1
]}

De Nuccio, Francesco ^{[2
]}

Mitolo, Vincenzo ^{[1
]}

Nicolardi, Giuseppe ^{[2
]}

Panaro, Maria Antonietta ^{[1
]}

机构：

[1] Univ Bari, Dept Human Anat & Histol, IT-70124 Bari, Italy

[2] Univ Salento, Sect Human Anat, Dept Biol & Environm Sci & Technol, Lecce, Italy

来源：

NEUROIMMUNOMODULATION | 2011年 / 18卷 / 02期

关键词：

Neuroinflammation; Parkinson's disease; 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine; Cytokines; IL-1; beta; TNF-alpha; IL-6; TUMOR-NECROSIS-FACTOR; PARKINSONS-DISEASE; INTERLEUKIN-1; RECEPTORS; DOPAMINERGIC NEUROTOXICITY; CEREBROSPINAL-FLUID; OXIDATIVE STRESS; NERVOUS-SYSTEM; GLIAL-CELLS; FACTOR TNF; MICE;

D O I：

10.1159/000320027

中图分类号：

R5 [内科学];

学科分类号：

1002 ; 100201 ;

摘要：

Parkinson's disease (PD) is a common neurodegenerative disease characterised by a slow and progressive degeneration of dopaminergic neurons in the substantia nigra (SN). Despite intensive research, the cause of neuronal loss in PD is poorly understood. Inflammatory mechanisms have been implicated in the pathophysiology of PD. In this study, conducted on an experimental 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) mouse model, we investigated the expression of interleukin (IL)-1 beta, tumor necrosis factor (TNF)-alpha, IL-6 and their receptors (IL-1RI, TNF-alpha RI, IL-6R alpha) at the SN and caudate-putamen (CP) levels. In MPTP-treated animals we observed a significant increase in IL-1 beta, TNF-alpha and IL-6 mRNA expression levels both in the SN and CP in comparison with untreated mice. In addition, both mRNA and protein levels of IL-1RI, TNF-alpha RI and IL-6R alpha were significantly enhanced in the SN of MPTP-treated mice in comparison to controls, whereas no significant differences were observed in the CP between treated and untreated mice. Overall, these results indicate a role of both pro-inflammatory cytokines and their receptors in the pathogenesis of PD. Copyright (C) 2010 S. Karger AG, Basel

引用

页码：79 / 88

页数：10

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