Protective Effect of Auricularia auricula Melanin on Iron Deficiency Anemia Induced Ulcerative Colitis in Mice

To explore the protective mechanism of Auricularia auricula melanin (AAM) on iron deficiency anemia (IDA) induced ulcerative colitis (UC) in mice.

Forty-five Kunming male mice were randomly divided into blank control group, model group, and AAM group (n = 15 each). The mice from all groups except the blank control one were provided with a low-iron diet to establish an IDA-induced UC model. After two weeks, AAM was administered by gavage to the mice from the AAM group for three weeks, whereas those from the model group continued receiving the low-iron diet. The effects of AAM on anemia indexes, colonic inflammation characteristics, oxidative stress, inflammatory factor expression levels and inflammatory signaling pathways in UC mice were evaluated.

Compared with the model group, the symptoms of anemia in the AAM group were alleviated. The body mass returned to the normal level, and the colonic pathological score was significantly reduced (P < 0.0001). In addition, the total antioxidant capacity (TAC) and superoxide dismutase (SOD) activity in the colon of mice from the AAM group were significantly enhanced compared with the model group (P < 0.0001), and the levels of malondialdehyde (MDA), hydroxyl radical (·OH), and superoxide anion radical (O₂^-·) were significantly decreased (P < 0.0001, P < 0.01, P < 0.001), indicating that AAM could enhance antioxidant capacity and attenuate oxidative damage in mice. Further mechanistic studies showed that intervention with AAM significantly regulated protein expression associated with Toll-like receptors-4/nuclear factor-kappa B (TLR4/NF-κB) signaling pathway, significantly down-regulated the gene expression of the pro-inflammatory cytokine tumor necrosis factor (TNF-α) (P < 0.01), and significantly increased the gene expression level of the anti-inflammatory cytokine interleukin-10 (IL-10) (P < 0.05).

Auricularia auricula melanin may regulate oxidative stress and inhibit the TLR4/NF-κB signaling pathway, thereby reducing intestinal mucosal ulcer, oxidative stress injury and inflammatory cell infiltration in colon tissue, and finally alleviating IDA-induced UC in mice.