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Neurosci Bull. 2018 Apr;34(2):270-282. doi: 10.1007/s12264-017-0188-0. Epub 2017 Nov 10.

Radio Electric Asymmetric Conveyer Technology Modulates Neuroinflammation in a Mouse Model of Neurodegeneration.

Author information

1
Department of Biosciences, Biotechnologies and Biopharmaceutics, University of Bari, Bari, Italy.
2
CNR Institute for Microelectronics and Microsystems, Via Monteroni (Campus Ecotekne), 73100, Lecce, Italy.
3
Department of Biological and Environmental Sciences and Technologies, Section of Human Anatomy, University of Salento, Lecce, Italy.
4
Department of Biological and Environmental Sciences and Technologies, Section of Human Anatomy, University of Salento, Lecce, Italy. dario.lofrumento@unisalento.it.
5
Neuropathology Unit, Institute of Experimental Neurology, Division of Neuroscience, IRCCS San Raffaele Scientific Institute, Via Olgettina 60, 20132, Milan, Italy.
6
Department of Mathematics and Physics, University of Salento, Via Arnesano, 73100, Lecce, Italy.
7
CNR Institute of Nanoscience NEST, Piazza San Silvestro 12, 56127, Pisa, Italy.
8
Department of Regenerative Medicine, Rinaldi Fontani Institute, Viale Belfiore 43, 50144, Florence, Italy.
9
Research Department, Rinaldi Fontani Foundation, Viale Belfiore 43, 50144, Florence, Italy.
10
IRF (Shanghai) Medical Sciences, 3000 Long Dong Avenue, Zhangjiang High-Tech Park, Shanghai, China.

Abstract

In this study, the effects of Radio Electric Asymmetric Conveyer (REAC), a non-invasive physical treatment, on neuroinflammatory responses in a mouse model of parkinsonism induced by intoxication with 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP), were investigated in vivo. We found that the REAC tissue optimization treatment specific for neuro-regenerative purposes (REAC TO-RGN-N) attenuated the inflammatory picture evoked by MPTP-induced nigro-striatal damage in mice, decreasing the levels of pro-inflammatory molecules and increasing anti-inflammatory mediators. Besides, there was a significant reduction of both astrocyte and microglial activation in MPTP-treated mice exposed to REAC TO-RGN-N. These results indicated that REAC TO-RGN-N treatment modulates the pro-inflammatory responses and reduces neuronal damage in MPTP-induced parkinsonism.

KEYWORDS:

Neurodegeneration; Neuroinflammation; Parkinson’s disease; REAC TO-RGN-N treatment

PMID:
29124672
PMCID:
PMC5856715
[Available on 2019-04-01]
DOI:
10.1007/s12264-017-0188-0
[Indexed for MEDLINE]

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