首页> 外文期刊>Carbohydrate Polymers: Scientific and Technological Aspects of Industrially Important Polysaccharides >Se-enriched G-frondosa polysaccharide protects against immunosuppression in cyclophosphamide-induced mice via MAPKs signal transduction pathway
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Se-enriched G-frondosa polysaccharide protects against immunosuppression in cyclophosphamide-induced mice via MAPKs signal transduction pathway

机译:富集的G-Frondosa多糖通过Mapks信号转导途径保护环磷酰胺诱导的小鼠免疫抑制

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摘要

To assess the immunomodulatory and antioxidant activities of a Se-polysaccharide from Se-enriched G. frondosa (Se-GFP-22), immunosuppressed mice models were generated by cyclophosphamide (CTX) administration and then treated with Se-GFP-22. Results showed that Se-GFP-22 could increase thymus and spleen indices, phagocytic index, co-mitogenic (ConA-or LPS-stimulated) activities on splenocytes, DTH reaction, serum hemolysin formation and immunoglobulin (Ig G, Ig A and Ig M) levels in CTX-treated mice. Se-GFP-22 significantly enhanced the antioxidant activity in CTX-treated mice, as shown by the evaluation of GSH-Px, SOD and CAT activities, as well as MDA levels in serum, liver and kidney. Se-GFP-22 strongly stimulated inflammatory cytokines (IL-2 and IFN-gamma) and NO productions by up-regulating mRNA expressions of IL-2, IFN-gamma and iNOS. Se-GFP- 22 possessed the immunomodulatory activity by up-regulating various transcription factors (JNK, ERK, and p38) in MAPKs signaling pathways. This study suggested that Se-GFP-22 may provide an alternative strategy in lessening chemotherapy-induced immunosuppression.
机译:为了评估来自Se-多糖的免疫调节和抗氧化活性来自Se-富集的G. Frondosa(Se-GFP-22),通过环磷酰胺(CTX)给药产生免疫抑制的小鼠模型,然后用SE-GFP-22处理。结果表明,SE-GFP-22可以增加脂肪细胞,第四次反应,血清溶血素形成和免疫球蛋白(Ig G,Ig A和Ig M的胸腺细胞,吞噬指数,Cona-Or促进)活性的胸腺和脾脏指数,吞噬指数,共同促致毒性(Cona-of或Lps刺激)活性(Ig G,Ig A和Ig m )CTX处理的​​小鼠中的水平。 SE-GFP-22显着增强了CTX处理的​​小鼠中的抗氧化活性,如GSH-PX,SOD和猫活动的评价所示,以及血清,肝肾的MDA水平。 Se-GFP-22强烈刺激的炎症细胞因子(IL-2和IFN-γ),通过UL-2,IFN-Gamma和InOS的UP调节mRNA表达没有生产。 SE-GFP-22通过在MAPKS信号通路中占据各种转录因子(JNK,ERK和P38)来拥有免疫调节活动。该研究表明,SE-GFP-22可以在减少化疗诱导的免疫抑制中提供替代策略。

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