No abstract

In this study, we investigated the immunostimulating activity of polysaccharides isolated from fruiting body of Inonotus obliquus (PFIO). Additionally, the signaling pathway of PFIO-mediated macrophage activation was investigated in RAW264.7 macrophage cells. We found that PFIO was capable of promoting NO/ROS production, TNF-α secretion and phagocytic uptake in macrophages, as well as cell proliferation, comitogenic effect and IFN-γ/IL-4 secretion in mouse splenocytes. PFIO was able to induce the phosphorylation of three MAPKs as well as the nuclear translocation of NF-κB, resulting in activation of RAW264.7 macrophages. PFIO also induced the inhibition of TNF-α secretion by anti-TLR2 mAb, consequently, PFIO might be involved in TNF-α secretion via the TLR2 receptor. In addition, our results showed that oral administration of PFIO suppressed in vivo growth of melanoma tumor in tumorbearing mice. In conclusion, our experiments presented that PFIO effectively promotes macrophage activation through the MAPK and NF-κB signaling pathways, suggesting that PFIO may potentially regulate the immune response.

Phellinus linteus, which is a traditional medicinal mushroom used in Asian countries for the treatment of various diseases, has attracted a lot of attention due to its antioxidant, anti-inflammatory, anti-mutagenicity, and cell-mediated immunity properties in addition to its ability to inhibit tumor growth and metastasis. However, the antidiabetic efficacy of P. linteus has not yet been examined. In this study, hispidin from P. linteus exhibited quenching effects against DPPH radicals, superoxide radicals, and hydrogen peroxide in a dose-dependent manner. Intracellular reactive oxygen species scavenging activity of hispidin was approximately 55% at a concentration of 30 microM. In addition, hispidin was shown to inhibit hydrogen peroxide-induced apoptosis and increased insulin secretion in hydrogen peroxide-treated cells. These combined results indicate that hispidin may act as an antidiabetic and that this property occurs through preventing beta-cells from the toxic action of reactive oxygen species in diabetes.