Myelin Protection by Ursolic Acid in Cuprizone-Induced Demyelination in Mice.

Fatemeh Honarvar, Vida Hojati, Nuredin Bakhtiari, Gholamhassan Vaezi, Mohammad Javan
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引用次数: 9

Abstract

Neuronal survival in multiple sclerosis (MS) and other demyelinating diseases depends on the preservation of myelin and remyelination of axons. Myelin protection is the main purpose to decrease myelin damage in the central nervous system (CNS). Ursolic acid (UA) as a natural product in apple is suggested to protect neural cells. This study is the first to demonstrate an effect for UA on CNS myelin loss induced by cuprizone toxin. In the current study, we hypothesized that daily treatment with UA in drinking water (1 mg/mL) prevents myelin damage by 6 weeks administration of CPZ in mice pellet which lead to corpus callosum axonal demyelination. We assessed the myelin content and the number of myelinating cells in corpus callosum by FluoroMyelin and luxol fast blue staining as well as by immunostaining against MBP and Olig2. Our finding indicated that UA could decrease the extent of demyelination area and enhanced myelin stain intensity within CC and protected oligodendrocyte lineage cells against cuprizone toxin. We could conclude that myelinated structures could be protected by UA in corpus callosum, which provide favorable evidence for the possibility of application of UA in demyelinating diseases and traumatic injuries.

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熊果酸对铜酮诱导小鼠脱髓鞘的保护作用。
多发性硬化症(MS)和其他脱髓鞘疾病的神经元存活依赖于髓鞘的保存和轴突的再髓鞘形成。髓磷脂保护是减少中枢神经系统髓磷脂损伤的主要目的。熊果酸作为苹果中的天然产物,被认为具有保护神经细胞的作用。本研究首次证实了UA对铜酮毒素诱导的中枢神经系统髓磷脂损失的影响。在本研究中,我们假设每天在饮用水中添加UA (1mg /mL)可以防止CPZ对小鼠颗粒造成髓鞘损伤,从而导致胼胝体轴突脱髓鞘。我们用FluoroMyelin和luxol快速蓝染色以及MBP和Olig2免疫染色评估胼胝体髓磷脂含量和髓鞘细胞数量。我们的研究结果表明,UA可以减少CC的脱髓鞘面积,增强髓磷脂染色强度,并保护少突胶质细胞系细胞免受铜酮毒素的侵害。由此可见,UA可保护胼胝体的髓鞘结构,为UA在脱髓鞘疾病和创伤性损伤中的应用提供了有利的证据。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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