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目的探讨黄芪糖蛋白(HQGP)对实验性自身免疫性脑脊髓炎(EAE)小鼠的治疗效果及可能机制。方法用髓鞘少突胶质细胞糖蛋白35-55(MOG35-55)诱导C57BL/6雌性小鼠建立EAE模型。分为黄芪糖蛋白治疗组和EAE对照组,隔天记录小鼠临床评分和体质量变化。HE染色和免疫荧光技术检测脊髓组织炎细胞浸润;MTT法检测细胞活性;Griess法检测一氧化氮(NO)释放;ELISA测定肿瘤坏死因子α(TNF-α)、白细胞介素6(IL-6)分泌,γ干扰素(IFN-γ)释放;流式细胞术检测CD4+T细胞亚群变化。结果 HQGP处理可减轻EAE症状,抑制中枢神经系统炎细胞浸润。抑制脾淋巴单核细胞活性、NO和TNF-α、IL-6分泌,促进IFN-γ的分泌。增加CD4+CD25+、CD4+IL-10+、CD4+IFN-γ+T细胞亚群的比例。结论 HQGP通过调节T细胞亚群比例,抑制炎症细胞因子释放,减轻EAE炎症反应。
Objective To investigate the therapeutic effect and possible mechanism of astragalus polysaccharide (HQGP) on experimental autoimmune encephalomyelitis (EAE) mice. Methods The C57BL / 6 female mice were induced by myelin oligodendrocyte glycoprotein 35-55 (MOG35-55) to establish an EAE model. Divided into astragalus glycosides treatment group and EAE control group, the other day recorded the clinical score and body weight changes in mice. HE staining and immunofluorescence were used to detect inflammatory cell infiltration in spinal cord tissue. Cell viability was measured by MTT assay. Nitric oxide (NO) release was assayed by Griess assay. Tumor necrosis factor-α (TNF-α), interleukin- ), IFN-γ release, and the change of CD4 + T cell subsets by flow cytometry. Results HQGP treatment could reduce the symptoms of EAE and inhibit the infiltration of central nervous system inflammatory cells. Inhibit splenic lymphocyte monocyte activity, secretion of NO and TNF-α and IL-6, and promote the secretion of IFN-γ. Increase the proportion of CD4 + CD25 +, CD4 + IL-10 +, CD4 + IFN-γ + T cell subsets. Conclusion HQGP can reduce the release of inflammatory cytokines and reduce the inflammatory response of EAE by regulating the proportion of T lymphocyte subsets.