BACKGROUND: Allergic asthma is an inflammatory disease resulting from continued or intermittent allergen exposure, and allergic rhinitis can be trigger of asthma . The main mechanism of these disease is allergic reaction and immune response dysregulation . Co-Q10 is an enzyme cofactor in mitochondria can control asthma and allergic rhinitis symptoms . In the present study, we determined that the CoQ10-induced anti-allergic effects were mediated by up-regulation of Nrf2 .
METHODS: Animal models of allergic rhinitis and allergic asthma were produced and treated with Co-Q10, Co-Q10 and O-3, Co-Q10 and Mg-S. Bronchoalveolar lavage fluid was collected from animal models, and IL-4, 5, 13, INF-y, Eicosanoids, IgE, EPO, and histamine production were measured . Also, COX-2, CCL24, CCL11, Nrf2, Eotaxin, Cytb, COX1 and ND1 genes expressions and histopathology were studied . BALf's cells were collected by tracheostomy and used in slide producing by cytospine . Cytokines, Eicosanoids, IgE, EPO, and histamine were measured by ELISA method . Gene expression was done by Real-time PCR .
RESULTS: Co-Q10 with two supplementation (Mg-S and O-3) modulate MRC, BALf eosinophils, eosinophilic inflammation related genes (eotaxin, CCL11 and CCL24), peribronchial and perivascular inflammation, EPO, type 2 cytokines (IL-4, 5 and 13), IgE, histamine, Cyc-LT and LTB4 as main allergic bio-factors . Importantly, Co-Q10 treatment increased Nrf2 expression and Nrf2 induced antioxidant genes, glutathione redox and inhibited inflammation, oxidative stress injury, Th2 cytokines production and attenuated allergic inflammatory responses.
CONCLUSION: Nrf2 is activated in response to allergen, induces resistance against the rhinitis and asthma development and plays an essential role in broncho-protection . Co-Q10 increases the Nrf2 expression and the Nrf2 over-expression has strong effect in control of type2 cytokines, allergic mediators and inflammatory factors that lead to harnessing of allergy and asthma.
Index: Allergy, Coenzyme, Cytokine, Immunoglobulin, Signaling, Th2