Protective effects of rutin through regulation of vascular endothelial growth factor in allergic rhinitis.

BACKGROUND

Allergic rhinitis (AR) is an allergic inflammatory disease induced by various mediators released by infiltrating inflammatory cells. Vascular endothelial growth factor (VEGF) increases the airway inflammatory response by promoting vascular permeability. Furthermore, it is known that Allium hookeri and one of its constituent compounds, rutin (RU), have anti-inflammatory, antioxidant, and antiplatelet effects.

OBJECTIVE

The aim of this study was to evaluate the regulation of AR by RU and A. hookeri.

METHODS

We assessed the therapeutic effects and the regulatory mechanisms of A. hookeri and RU on phorbol 12-myristate 13-acetate plus A23187 (PMACI) stimulated human mast cell line (HMC) 1 cells, and ovalbumin (OVA) sensitized mouse model of AR.

RESULTS

A. hookeri and RU significantly inhibited the production and messenger RNA (mRNA) expression of VEGF in PMACI-stimulated HMC-1 cells and significantly decreased VEGF levels in our murine AR model. The increased rubs scores and immunoglobulin E and interleukin (IL) 4 levels in OVA-sensitized mice were significantly reduced by the administration of A. hookeri, and RU significantly inhibited the production and mRNA expression and RU. Also, A. hookeri and RU significantly reduced IL-4 and IL-5 production in OVA-stimulated splenocytes. Furthermore, A. hookeri and RU significantly decreased chemokine levels (intercellular adhesion molecule-1, macrophage inflammatory protein-2) in nasal mucosa tissues. In the mouse AR model, A. hookeri and RU significantly prevented eosinophil and mast cell infiltration and reduced inflammatory cytokine levels induced by OVA sensitization. In addition, A. hookeri and RU significantly reduced mast cell-derived caspase-1 activity in OVA-sensitized mice.

CONCLUSION

The present study showed that A. hookeri or RU had an anti-allergic inflammatory effects. Analysis of these results indicated that A. hookeri and RU might protect against AR.