A novel polysaccharide, here named DP1, was isolated from the fruiting body of Dictyophora indusiata using a water extraction method. Structure characterization revealed that DP1 had an average molecular weight of 1132 kDa and consisted of glucose (56.2%), galactose (14.1%), and mannose (29.7%). The main linkage type of DP1 were proven to be (1 → 3)-linked α-l-Man, (1 → 2,6)-linked α-d-Glc, (1 → 6)-linked β-d-Glc, (1 → 6)-linked β-d-Gal, and (1 → 6)-linked β-d-Man by periodate oxidation–Smith degradation and nuclear magnetic resonance analysis. The immunostimulating assay indicated that DP1 could significantly promote macrophage NO, TNF-α, and IL-6 secretion in murine RAW 264.7 cells involving complement receptor 3 (CR3). The immune activities of DP1 were quite stable under thermal processing (100, 121, and 145 °C). Besides, DP1 retained stability after acidic/alkline treatment (pH 4.0–10.0), which enabled it to be an ideal complementary medicine or functional food for therapeutics of hypoimmunity and immunodeficiency diseases.

Dictyophora indusiata polysaccharide (DP1) was successfully chelated with zinc chloride to achieve its enhanced antiproliferative activity. The obtained DP1–Zn complex showed significant antiproliferative activity (18.1 ± 2.84% viability of MCF-7 cells at 250 μg/mL) on a group of human cancer cell lines through induction of apoptosis. The pro-apoptotic action of DP1–Zn was confirmed by morphological changes including chromatin condensation, DNA breakage, and S phase cell cycle arrest in human breast adenocarcinoma cells (MCF-7). The DP1–Zn-induced apoptotic pathways were characterized by the activation of caspases-3, -8, and -9, mitochondrial dysfunction, and reactive oxygen species (ROS) overproduction (305 ± 7.06% production of control at 250 μg/mL). This study suggested that DP1–Zn can be developed as a candidate for cancer treatment and prevention, especially human breast adenocarcinoma.

The intracellular antioxidant activities of diosmetin were evaluated by cellular antioxidant activity (CAA) assay, 2,2-azobis(2-amidinopropane) dihydrochloride (AAPH)-induced erythrocyte hemolysis assay and cupric chloride (CuCl2)-induced plasma oxidation assay. The results showed that diosmetin exhibits strong cellular antioxidant activity (EC50 = 7.98 μmol, CAA value = 58 μmol QE/100 μmol). It was also found that diosmetin treatment could effectively attenuate AAPH-induced erythrocyte hemolysis (91.0% inhibition at 100 μg/mL) and CuCl2-induced plasma oxidation through inhibition of intracellular reactive oxygen species (ROS) generation. Diosmetin could significantly restore AAPH-induced increase of intracelluar antioxidant enzyme (SOD, GPx, and CAT) activities to normal levels, as well as inhibit intracellular malondialdehyde (MDA) formation. Thus, the intracellular antioxidant detoxifying mechanism of diosmetin is associated with both nonenzymatic and enzymatic defense systems.