Format

Send to

Choose Destination
J Neuroinflammation. 2018 Aug 31;15(1):249. doi: 10.1186/s12974-018-1266-6.

Vitamin D protects dopaminergic neurons against neuroinflammation and oxidative stress in hemiparkinsonian rats.

Author information

1
Faculty of Medicine, Federal University of Ceará (UFC), Rua Barbosa de Freitas, 130/1100, Fortaleza, CE, 60170-020, Brazil.
2
Faculty of Medicine Estácio of Juazeiro do Norte (Estácio/FMJ), Juazeiro do Norte, Brazil.
3
Federal University of Piauí (UFPI), Picos, Brazil.
4
Faculty of Medicine, Federal University of Ceará (UFC), Rua Barbosa de Freitas, 130/1100, Fortaleza, CE, 60170-020, Brazil. gbviana@live.com.

Abstract

BACKGROUND:

The deficiency in 1α, 25-dihydroxyvitamin D3 (VD3) seems to increase the risk for neurodegenerative pathologies, including Parkinson's disease (PD). The majority of its actions are mediated by the transcription factor, VD3 receptor (VD3R).

METHODS:

The neuroprotective effects of VD3 were investigated on a PD model. Male Wistar rats were divided into the following groups: sham-operated (SO), 6-OHDA-lesioned (non-treated), and 6-OHDA-lesioned and treated with VD3 (7 days before the lesion, pre-treatment or for 14 days after the 6-OHDA striatal lesion, post-treatment). Afterwards, the animals were subjected to behavioral tests and euthanized for striatal neurochemical and immunohistochemical assays. The data were analyzed by ANOVA and the Tukey test and considered significant for p < 0.05.

RESULTS:

We showed that pre- or post-treatments with VD3 reversed behavioral changes and improved the decreased DA contents of the 6-OHDA group. In addition, VD3 reduced the oxidative stress, increased (TH and DAT), and reduced (TNF-alpha) immunostainings in the lesioned striata. While significant decreases in VD3R immunoreactivity were observed after the 6-OHDA lesion, these changes were blocked after VD3 pre- or post-treatments. We showed that VD3 offers neuroprotection, decreasing behavioral changes, DA depletion, and oxidative stress. In addition, it reverses partially or completely TH, DAT, TNF-alpha, and VD3R decreases of immunoreactivities in the non-treated 6-OHDA group.

CONCLUSIONS:

Taken together, VD3 effects could result from its anti-inflammatory and antioxidant actions and from its actions on VD3R. These findings should stimulate translational research towards the VD3 potential for prevention or treatment of neurodegenerative diseases, as PD.

KEYWORDS:

Neuroinflammation; Oxidative stress; Parkinson’s disease and neurodegeneration; Vitamin D; Vitamin D receptors

PMID:
30170624
PMCID:
PMC6119240
DOI:
10.1186/s12974-018-1266-6
[Indexed for MEDLINE]
Free PMC Article

Supplemental Content

Full text links

Icon for BioMed Central Icon for PubMed Central
Loading ...
Support Center