Nevadensin relieves food allergic responses and passive cutaneous anaphylaxis in mice through inhibiting the expression of c-Kit receptors.

Nevadensin (NEV), a natural flavonoid compound derived from Lysionotus pauciflorus Maxim, has numerous biological activities. However, few researchers have examined its potential impact on alleviating allergies. In the present study, NEV was found to upregulate rectal temperature, suppress the development of diarrhea, and decrease the levels of serum specific immunoglobulin E, histamine and mouse MC protease-1 in ovalbumin-allergic mice. Moreover, NEV also alleviated passive cutaneous anaphylaxis reactions and inhibited the release of ß-hexosaminidase and histamine in bone marrow-derived mast cells. Furthermore, we provide the first demonstration that NEV decreases the expression of c-Kit and suppresses the proliferation of bone marrow-derived mast cells and accelerates their apoptosis. These findings indicated that L. pauciflorus-derived NEV might have the potential to alleviate food hypersensitivity.

Viridicatol Isolated from Deep-Sea Penicillium Griseofulvum Alleviates Anaphylaxis and Repairs the Intestinal Barrier in Mice by Suppressing Mast Cell Activation.

Viridicatol is a quinoline alkaloid isolated from the deep-sea-derived fungus Penicillium griseofulvum. The structure of viridicatol was unambiguously established by X-ray diffraction analysis. In this study, a mouse model of ovalbumin-induced food allergy and the rat basophil leukemia (RBL)-2H3 cell model were established to explore the anti-allergic properties of viridicatol. On the basis of the mouse model, we found viridicatol to alleviate the allergy symptoms; decrease the levels of specific immunoglobulin E, mast cell protease-1, histamine, and tumor necrosis factor-α; and promote the production of interleukin-10 in the serum. The treatment of viridicatol also downregulated the population of B cells and mast cells (MCs), as well as upregulated the population of regulatory T cells in the spleen. Moreover, viridicatol alleviated intestinal villi injury and inhibited the degranulation of intestinal MCs to promote intestinal barrier repair in mice. Furthermore, the accumulation of Ca2+ in RBL-2H3 cells was significantly suppressed by viridicatol, which could block the activation of MCs. Taken together, these data indicated that deep-sea viridicatol may represent a novel therapeutic for allergic diseases.

Dihydromyricetin inhibited ovalbumin-induced mice allergic responses by suppressing the activation of mast cells.

Dihydromyricetin (DMY) is a natural flavonoid compound derived from Lysionotus pauciflorus Maxim and has been found to possess numerous biological activities. However, there have been few reports regarding its anti-food allergic activity. In this study, we demonstrated that DMY could upregulate the rectal temperature, suppress the development of diarrhea, decrease the levels of serum specific immunoglobulin (Ig)E, histamine, and mouse mast cell protease-1, and promote the production of interleukin-10 in ovalbumin-allergic mice. Moreover, DMY downregulated the population of B cells and mast cells and upregulated the population of regulatory T cells in the spleens of ovalbumin-allergic mice. Furthermore, DMY blocked the high affinity IgE receptor (FcεRI)-IgE interaction, inhibited the release of ß-hexosaminidase and histamine in rat basophilic leukemia-2H3 cells, and alleviated passive cutaneous anaphylaxis reactions. These findings indicated that L. pauciflorus derived DMY might have the potential to alleviate food hypersensitivity or allergic diseases.