Previous studies have shown that Huangqi glycoprotein (HQGP) has an anti-inflammatory effect in vitro, and suppressed experimental autoimmune encephalomyelitis (EAE), an animal model of multiple sclerosis; however, the mechanism underlying its effect is largely unknown. In this manuscript we investigated the mechanisms by which HQGP protect mice from EAE. HQGP was extracted from Astragalus membranaceus and purified by anion-exchange and gel filtration chromatography. HQGP delayed disease onset, reduced disease severity and alleviated inflammation and demyelination in the central nervous system (CNS). Moreover, HQGP reduced the infiltration of pathogenic immune cells and increased the expression of microtubule-associated protein 2 (MAP-2) and neuronal nuclei (NeuN) in the CNS. HQGP treatment also reduced the expression of chemokines such as CCL2 and CCL5 and the production of tumor necrosis factor α (TNF-α), interleukin (IL)-1β, IL-6, but increased the level of IL-10. These results demonstrate that HQGP suppressed EAE development by modulating the immune system and the infiltration of leukocytes to the CNS as well as promoting axon and neural repair.

中文翻译：

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黄芪糖蛋白治疗实验性自身免疫性脑脊髓炎的免疫调节和神经保护机制。

先前的研究表明，黄芪糖蛋白（HQGP）在体外具有抗炎作用，并能抑制多发性硬化动物模型实验性自身免疫性脑脊髓炎（EAE）。但是，影响其作用的机制在很大程度上尚不清楚。在本手稿中，我们研究了HQGP保护小鼠免受EAE侵害的机制。从黄芪中提取HQGP，并通过阴离子交换和凝胶过滤色谱法纯化。HQGP延缓了疾病的发作，降低了疾病的严重程度，减轻了中枢神经系统（CNS）的炎症和脱髓鞘。此外，HQGP减少了中枢神经系统中病原性免疫细胞的浸润，并增加了微管相关蛋白2（MAP-2）和神经元核（NeuN）的表达。HQGP治疗还降低了趋化因子例如CCL2和CCL5的表达以及肿瘤坏死因子α（TNF-α），白介素（IL）-1β，IL-6的产生，但是增加了IL-10的水平。这些结果表明，HQGP通过调节免疫系统和白细胞向CNS的浸润以及促进轴突和神经修复来抑制EAE的发展。