Vitamin D protects dopaminergic neurons against neuroinflammation and oxidative stress in hemiparkinsonian rats.
Vitamin D protects dopaminergic neurons against neuroinflammation and oxidative stress in hemiparkinsonian rats.
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DOI：
10.1186/s12974-018-1266-6
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发表时间：
2018-08-31
影响因子：
9.3
通讯作者：
Viana GSB
中科院分区：
文献类型：
--
作者：
Lima LAR;Lopes MJP;Costa RO;Lima FAV;Neves KRT;Calou IBF;Andrade GM;Viana GSB
缺乏1 α，25-二羟维生素D3（VD3）似乎会增加神经退行性病变的风险，包括帕金森病（PD）。它的大部分作用是由转录因子VD3受体（VD3R）介导的。在PD模型上研究VD3的神经保护作用。将雄性Wistar大鼠分为以下组：假手术组（SO）、6-OHDA损伤组（未处理组）和6-OHDA损伤并用VD3处理组（损伤前7天，处理前或6-OHDA纹状体损伤后14天，处理后）。之后，对动物进行行为测试并安乐死以进行纹状体神经化学和免疫组织化学测定。通过ANOVA和Tukey检验分析数据，并认为p <0.05是显著的。我们发现，用VD3预处理或后处理逆转了6-OHDA组的行为变化，并改善了DA含量的下降。此外，VD3减少了氧化应激，增加（TH和DAT），并减少（TNF-α）在受损的纹状体免疫染色。虽然在6-OHDA损伤后观察到VD3R免疫反应性显著降低，但这些变化在VD3预处理或后处理后被阻断。我们发现VD3提供神经保护，减少行为变化，DA消耗和氧化应激。此外，它部分或完全逆转未处理的6-OHDA组中TH、DAT、TNF-α和VD3R免疫反应性的降低。总之，VD3的作用可能是由于其抗炎和抗氧化作用以及其对VD3R的作用。这些发现应该刺激对VD3预防或治疗神经退行性疾病（如PD）的潜力的转化研究。本文的在线版本（10.1186/s12974 - 018 - 1266 - 6）包含补充材料，可供授权用户使用。
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). 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. 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. 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. The online version of this article (10.1186/s12974-018-1266-6) contains supplementary material, which is available to authorized users.
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影响因子：
--
作者：
Ayala A;Muñoz MF;Argüelles S
通讯作者：
Argüelles S
影响因子：
--
作者：
GASCONBARRE, M;HUET, PM
通讯作者：
HUET, PM
影响因子：
2.9
作者：
ALTEMUS, KL;FINGER, S;BIRGE, SJ
通讯作者：
BIRGE, SJ
影响因子：
4.1
作者：
Cui, Xiaoying;Gooch, Helen;Eyles, Darryl
通讯作者：
Eyles, Darryl
影响因子：
2.9
作者：
Blesa J;Trigo-Damas I;Quiroga-Varela A;Jackson-Lewis VR
通讯作者：
Jackson-Lewis VR