Immunomodulatory and neuroprotective mechanisms of Huangqi glycoprotein treatment in experimental autoimmune encephalomyelitis

• Published in: Folia neuropathologica Vol. 57; no. 2; pp. 117 - 128
• Main Authors: Xing, Yanxia, Liu, Binyu, Zhao, Yijin, Zhang, Lihong, Thome, Rodolfo, Xue, Huiqing, Zhang, Peijun, Ma, Cungen
• Format: Journal Article
• Language: English
• Published: Poland Termedia sp. z o.o 01.01.2019; Termedia Publishing House
• Subjects: Animal models; Animals; Central nervous system; Chemokines; Chemokines - metabolism; Cytokines - metabolism; Demyelination; Drugs, Chinese Herbal - pharmacology; Drugs, Chinese Herbal - therapeutic use; Encephalomyelitis, Autoimmune, Experimental - drug therapy; Encephalomyelitis, Autoimmune, Experimental - metabolism; Experimental allergic encephalomyelitis; experimental autoimmune encephalomyelitis; Female; Glycoproteins; huangqi glycoprotein; Immune system; immunocyte; Immunomodulation; Inflammation; Interleukin 10; Interleukin 6; Leukocytes; Metastases; Mice; Microtubule-associated protein 2; Monocyte chemoattractant protein 1; Multiple sclerosis; nerve repair; Neuroprotection; Neuroprotective Agents - pharmacology; Neuroprotective Agents - therapeutic use; Severity of Illness Index; Tumor necrosis factor-TNF; Tumor necrosis factor-α; nerve repair; experimental autoimmune encephalomyelitis; chemokines; Huangqi glycoprotein; immunocyte
• ISSN: 1641-4640; 1509-572X
• DOI: 10.5114/fn.2019.85843

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.