Apigenin attenuates PM2.5-induced airway hyperresponsiveness and inflammation by down-regulating NF-κB in murine model of asthma.

The purpose of this study was to investigate the anti-inflammatory potential of the natural flavonoid apigenin to mitigate the airway inflammation in asthmatic mice exposed to particulate matter (PM) 2.5, and examine the possible mechanisms involved. BALB/c mice were sensitized and challenged with ovalbumin (OVA), then administered apigenin at a dose of 20 mg/kg/day, followed by PM2.5 exposure at a dose of 100 μg/mouse before prior to each challenge. The results showed that PM2.5 exposure aggravated airway hyper-responsiveness (AHR) and led to a mixed T helper (Th)2 cell/interleukin (IL)-17 response in asthmatic mice. Apigenin treatment markedly decreased both AHR and the percentage of eosinophils, as well as neutrophil infiltration in the bronchoalveolar lavage fluid (BALF) and lung tissue of OVA-sensitized and PM2.5-exposed mice. There were significant reductions in the levels of total serum immunoglobulin IgE and T-helper cell type 2 (Th2)-related cytokines (IL-4, IL-13) and Th17-related cytokine IL-17 in BALF. In addition, treatment with apigenin down-regulated the expression of nuclear factor kappa-light -chain-enhancer of activated B cells (NF-κB) p65 submit in lung tissue of asthmatic mice. These data suggest that apigenin exhibited both anti-allergic and anti-neutrophil-related inflammatory activity in a murine asthma model exposed to PM2.5, possibly through modulating IL-17 and down-regulating the expression of NF-κB. Thus, apigenin may be a promising candidate for preventing PM2.5 exposure-enhanced pre-existing asthma. IJCEP