| Literature DB >> 25773147 |
Chao Zhen1, Xuedan Feng1, Zhe Li2, Yabo Wang3, Bin Li4, Lin Li1, Moyuan Quan1, Gaoning Wang1, Li Guo5.
Abstract
Multiple sclerosis (MS) has been associated with a history of sub-optimal exposure to ultraviolet light, implicating vitamin D3 as a possible protective agent. We evaluated whether 1,25(OH)2D3 attenuates the progression of experimental autoimmune encephalomyelitis (EAE), and explored its potential mechanisms. EAE was induced in C57BL/6 mice via immunization with MOG35-55, and some mice received 1,25(OH)2D3. 1,25(OH)2D3 inhibited EAE progression. Additionally, 1,25(OH)2D3 reduced inflammation, demyelination, and neuron loss in the spinal cord. The protective effect of 1,25(OH)2D3 was associated with significantly elevated expression of Beclin1, increased Bcl-2/Bax ratio, and decreased LC3-II accumulation. Thus, 1,25(OH)2D3 may represent a promising new MS treatment.Entities:
Keywords: 1,25(OH)(2)D(3); Apoptosis; Autophagy; Experimental autoimmune encephalomyelitis; Multiple sclerosis
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Year: 2015 PMID： 25773147 DOI： 10.1016/j.jneuroim.2015.01.012
Source DB: PubMed Journal: J Neuroimmunol ISSN： 0165-5728 Impact factor: 3.478