Iron deficiency anemia (IDA) is a common iron deficiency disease. IDA has become one of the major public health problems worldwide. Our previous studies have shown that Auricularia auricula melanin (AAM) can alleviate IDA, but the mechanism is not clear. In this study, the role of the intestinal microflora in the improvement of IDA by AAM was studied by elimination of gut bacteria using an antibiotic cocktail as well as using metabonomics. The results showed that AAM treatment significantly alleviated anemia symptoms of IDA mice in terms of body mass, hemoglobin concentration, hematocrit, mean erythrocyte volume and platelet count, and this effect was lost when the intestinal flora was eliminated. Totally 76 differential metabolites were identified by metabolnomics analysis. Pathway enrichment analysis identified seven pathways including tryptophan metabolism, phenylalanine, tyrosine and tryptophan biosynthesis, ascorbic and uronic metabolism, glutathione metabolism, tyrosine metabolism, pentose and glucuronate interconversion and steroid hormone biosynthesis. Among these, tryptophan metabolism was most significant. In the presence of intestinal microflora, tryptophan metabolites such as 5-hydroxyindole acetic acid and N-formyl kynurenine were significantly accumulated in IDA mice supplemented with AAM, indicating that AAM could mitigate IDA, which may be related to activation of tryptophan metabolism through the intestinal flora. This study may provides a theoretical basis for further research on the mechanisms by which AAM improves IDA and for the development of anti-IDA products.
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Open Access
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Open Access
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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.
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