Zhen Chao, Feng Xuedan, Li Zhe, Wang Yabo, Li Bin, Li Lin, Quan Moyuan, Wang Gaoning, Guo Li
Department of Neurology, The Second Hospital of Hebei Medical University, Shijiazhuang, 050000 Hebei, China.
Department of Neurology, Hebei General Hospital, Shijiazhuang, 050051 Hebei, China.
J Neuroimmunol. 2015 Mar 15;280:1-7. doi: 10.1016/j.jneuroim.2015.01.012. Epub 2015 Jan 29.
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.
多发性硬化症（MS）与紫外线暴露不足的病史有关，这表明维生素D3可能是一种保护剂。我们评估了1,25(OH)2D3是否能减缓实验性自身免疫性脑脊髓炎（EAE）的进展，并探讨了其潜在机制。通过用MOG35-55免疫在C57BL/6小鼠中诱导EAE，一些小鼠接受1,25(OH)2D3。1,25(OH)2D3抑制了EAE的进展。此外，1,25(OH)2D3减少了脊髓中的炎症、脱髓鞘和神经元损失。1,25(OH)2D3的保护作用与Beclin1表达显著升高、Bcl-2/Bax比值增加以及LC3-II积累减少有关。因此，1,25(OH)2D3可能是一种有前景的新型MS治疗方法。
