Ganoderma atrum polysaccharide ameliorates ROS generation and apoptosis in spleen and thymus of immunosuppressed mice
Ganoderma atrum polysaccharide (PSG-1) is a bioactive compound with antioxidant and immunomodulatory activities. The aim of this study was to determine the effect of PSG-1 on reactive oxygen species (ROS) generation and apoptosis in spleen and thymus of cyclophosphamide (CTX)-induced immunosuppresse...
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Veröffentlicht in: | Food and chemical toxicology 2017-01, Vol.99, p.199-208 |
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Sprache: | eng |
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Zusammenfassung: | Ganoderma atrum polysaccharide (PSG-1) is a bioactive compound with antioxidant and immunomodulatory activities. The aim of this study was to determine the effect of PSG-1 on reactive oxygen species (ROS) generation and apoptosis in spleen and thymus of cyclophosphamide (CTX)-induced immunosuppressed mice. The results showed that PSG-1 protected mice against CTX-mediated immunosuppression, as evidenced by enhancing the ratios of thymus and spleen weights to body weight, promoting T cell and B cell survival, and increasing levels of TNF-α and IL-2. Apoptosis, ROS generation and lipid peroxidation in the immune organs of the immunosuppressed animals were ameliorated by PSG-1. The immune benefits of PSG-1 were associated with the enhancement of the activities of glutathione peroxidase, superoxide dismutase and catalase in the immune organs, implying that antioxidant activities of PSG-1 may play an important role in PSG-1-evoked immune protection. Taken together, these findings have demonstrated that PSG-1 may ameliorate CTX-induced immunosuppression through reducing apoptosis and oxidative damage in immunological system.
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•PSG-1 protected mice against CTX-mediated immune dysfunction in vivo.•PSG-1 ameliorated oxidative damage in spleen and thymus of immunosuppressed mice.•PSG-1 ameliorated apoptosis in spleen and thymus of immunosuppressed mice.•Antioxidant activities play an important role in PSG-1-triggered immune benefits in immunosuppressed mice. |
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ISSN: | 0278-6915 1873-6351 |
DOI: | 10.1016/j.fct.2016.11.033 |