Multiple sclerosis (MS) is an immune-mediated demyelinating disorder in the central nervous system (CNS) with no definitive treatment, but it can be alleviated by changing life habits. Calorie restriction (CR) is effective in preventing or treating metabolic and autoimmune disorders. CR is one of the helpful approaches to control the progression of MS. In the present study, we investigated the preventive effect of caloric restriction on cuprizone induced-demyelination, a model of multiple sclerosis. To induce acute demyelination in C57/BL6 mice, we added 0.2% Cuprizone (CPZ) to their diet for 6 weeks. To induce calorie restriction, 10% Carboxymethyl cellulose (CMC) was added to the diet as a dietary cellulose fiber for 6 weeks. Remyelination was studied by luxol fast blue (LFB) staining. Microglia activity, M1 and M2 microglial/macrophage phenotypes were assessed by immunohistochemistry of Iba-1, iNOS and Arg‐1, respectively. The expression of targeted genes was assessed by the real‐time polymerase chain reaction. Luxol fast blue (LFB) staining showed that the CR regimen could decrease the cuprizone-induced demyelination process (p < 0.01). Moreover, the CR application could improve balance and motor performance in cuprizone-intoxicated mice by significantly enhancing protein and gene expression of Sirt1, M2 microglial phenotype marker (Arg-1) and Akt1 gene expression, also decreased M1 microglial phenotype marker (iNOS), Akt2 and P53 gene expressions (p < 0.05). Cumulatively, it can be concluded that caloric restriction was able to counteract MS symptoms through alleviating inflammatory responses.

多发性硬化症 (MS) 是一种免疫介导的中枢神经系统 (CNS) 脱髓鞘疾病，目前尚无明确的治疗方法，但可以通过改变生活习惯来缓解。热量限制 (CR) 可有效预防或治疗代谢和自身免疫性疾病。CR 是控制 MS 进展的有用方法之一。在本研究中，我们研究了热量限制对多发性硬化模型铜酮诱导脱髓鞘的预防作用。为了在 C57/BL6 小鼠中诱导急性脱髓鞘，我们在它们的饮食中添加了 0.2% Cuprizone (CPZ) 6 周。为了诱导热量限制，将 10% 羧甲基纤维素 (CMC) 作为膳食纤维素纤维添加到饮食中，持续 6 周。通过 luxol fast blue (LFB) 染色研究髓鞘再生。小胶质细胞活动，M1 和 M2 小胶质细胞/巨噬细胞表型分别通过 Iba-1、iNOS 和 Arg-1 的免疫组织化学进行评估。通过实时聚合酶链反应评估靶基因的表达。Luxol fast blue (LFB) 染色显示 CR 方案可以减少铜宗诱导的脱髓鞘过程 (p < 0.01)。此外，CR 应用可通过显着增强 Sirt1、M2 小胶质细胞表型标志物 (Arg-1) 和 Akt1 基因表达的蛋白质和基因表达，同时降低 M1 小胶质细胞表型标志物 (iNOS) 来改善铜宗中毒小鼠的平衡和运动表现， Akt2 和 P53 基因表达 (p < 0.05)。累积起来，可以得出结论，热量限制能够通过减轻炎症反应来抵消 MS 症状。