紅麴代謝產物 monascin 與 ankaflavin 對於過敏反應中肥大細胞與 T 細胞之影響

Type I allergy includes asthma, food allergy, urticaria and so on. Its prevalence increases with industrialized and modernized lifestyles. The mechanism of type I allergy began with antigen presenting cells (APCs) contacting with allergens, and then APCs recognize, engulfe, and present antigen to naive T cells, which make T cells activated and differentiated. In allergic patients, T cells tended to differentiate into T helper 2 (Th2) cells. Th2 released cytokines included interleukin-4 (IL-4), IL-5, and IL-13 that turn B cells into IgE-releasing plasma cells. The produced IgE bound to IgE receptors on mast cells. As a result, when next time allergy patients contact the same allergen, allergen would cross-link with IgE which is previously bound on mast cells, followed with the activation and inflammatory mediator-secretion of mast cells. These turned out making patients bronchial constriction, diarrhea, and wheal-and-flare reaction. In previous study, treating with Monascus secondary metabolites monascin and ankaflavin to ovalbumin-induced BALB/c mice could ameliorate allergic airway inflammation. It is showed that monascin and ankaflavin may have the anti-asthma potential. In order to know the improving mechanism of monascin and ankaflavin related to which immune cells, our lab investigated the influence of monascin on the APCs dendritic cells and EL4 T cells. We discovered that monascin inhibited the maturation of dendritic cells and reduced the Th2 cytokines release of EL4 T cell. However, the effects of ankaflavin on EL4 T cell and both monascin and ankaflavin on mast cells haven’t been investigated. Therefore, we hope to understand the impact of monascin and ankaflavin on these two cells. According to the results, we found that ankaflavin could reduce the production of PMA/ionomycin-induced Th1 and Th2 cytokine, and may possess anti-inflammatory potential. In RBL-2H3 mast cells, both monasin and ankaflavin (40 μM) decrease PMA/ionomycin-induced mast cell tumor necrosis factor α (TNF-α) release and degranulation. As we further examined the possible mechanism, the results showed that monascin and ankaflavin had no influence over intracellular calcium and reactive oxygen species (ROS) level. Nonetheless, monascin and ankaflvin could improve mast cell activation by controlling the activation and phosphorylation of protein kinase C (PKC) and mitogen-activated protein kinase (MAPK) family ERK, JNK, and p38. To sum up, monascin and ankaflavin had regulating effects on the generation of T cell cytokines and mast cell inflammatory mediators. Both may own the potential to improve type I allergy.