Se-enriched G. frondosa polysaccharide protects against immunosuppression in cyclophosphamide-induced mice via MAPKs signal transduction pathway
•Se-GFP-22 protected against the immunosuppression effects caused by CTX.•Se-GFP-22 restored the oxidative stress caused by CTX.•Se-GFP-22 up-regulated the mRNA expressions of IL-2, IFN-γ and iNOS in splenocytes.•Se-GFP-22-induced splenocytes activation is regulated via MAPKs signaling pathways.•Se-...
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Veröffentlicht in: | Carbohydrate polymers 2018-09, Vol.196, p.445-456 |
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Hauptverfasser: | , , , , , , , , , , |
Format: | Artikel |
Sprache: | eng |
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Zusammenfassung: | •Se-GFP-22 protected against the immunosuppression effects caused by CTX.•Se-GFP-22 restored the oxidative stress caused by CTX.•Se-GFP-22 up-regulated the mRNA expressions of IL-2, IFN-γ and iNOS in splenocytes.•Se-GFP-22-induced splenocytes activation is regulated via MAPKs signaling pathways.•Se-GFP-22 have great potential as the adjuvant chemotherapy agent of cancer.
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-γ) and NO productions by up-regulating mRNA expressions of IL-2, IFN-γ 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. |
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ISSN: | 0144-8617 1879-1344 |
DOI: | 10.1016/j.carbpol.2018.05.046 |