Dietary supplementation of vitamin D is commonly recommended to patients with multiple sclerosis. We recently found that high-dose of the hormonally active 1,25-dihydroxyvitamin-D₃ (1,25D) promotes myelin repair in the cuprizone model for de- and remyelination. In the present study, we quantified 5062 proteins, of which 125 were differentially regulated in brain tissue from 1,25D treated mice during remyelination, compared to placebo. Proteins upregulated in the early remyelination phase were involved in calcium binding, e.g. calretinin (>1.3 fold, p < 0.005), S10A5 and secretagogin, and involved in mitochondrial function, e.g. NADH-ubiquinone oxidoreductase chain 3, and acyl-coenzyme A synthetase. Calretinin, S10A5 and secretagogin expression levels were characterized using immunohistochemistry. Calretinin immunoreactivity was significantly increased (>3 fold, p = 0.016) in the medial septal nuclei of 1,25D treated mice in the early remyelination phase. Our results indicate that vitamin D may influence remyelination by mechanisms involving an increase in calretinin expression and potentially other calcium binding proteins.

通常建议多发性硬化症患者饮食中补充维生素D。我们最近发现，高剂量的具有激素活性的1,25-二羟基维生素D ₃（1,25D）可促进cuprizone模型中髓磷脂的修复，从而实现脱髓鞘和再髓鞘化。在本研究中，我们量化了5062种蛋白质，与安慰剂相比，在髓鞘再生过程中1,25D处理的小鼠的脑组织中有125种蛋白质受到差异调节。在早期髓鞘再生阶段上调的蛋白质参与钙结合，例如钙黄蛋白（> 1.3倍，p <0.005），S10A5和促分泌素，并参与线粒体功能，例如NADH-泛醌氧化还原酶链3和酰基辅酶A合成酶。钙卫蛋白，S10A5和secretagogin表达水平使用免疫组织化学进行了表征。在早期髓鞘再生阶段，在1,25D处理的小鼠的中隔核中，钙网蛋白的免疫反应性显着增加（> 3倍，p = 0.016）。