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Apigenin attenuates PM2.5-induced airway hyperresponsiveness and inflammation by down-regulating NF-κB in murine
Lingling Pang1,2, Shenchun Zou2, Ying Shi3
1Shandong University Jinan 250100, Shandong Province, China.
Abstract:
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.
Insights
Apigenin, a natural flavonoid, reduces airway inflammation and hyper-responsiveness in mice with asthma exposed to particulate matter (PM) 2.5. It works by modulating T-helper cell responses and down-regulating NF-κB, suggesting potential for asthma management.
Area of Science:
- Immunology
- Environmental Health
- Pharmacology
Background:
- Asthma is a chronic respiratory disease exacerbated by air pollutants like particulate matter (PM) 2.5.
- PM2.5 exposure can worsen airway inflammation, hyper-responsiveness, and allergic responses in asthmatic individuals.
- Natural compounds are being investigated for their therapeutic potential against environmentally-induced asthma exacerbations.
Purpose of the Study:
- To investigate the anti-inflammatory effects of apigenin on airway inflammation in a murine model of asthma.
- To determine if apigenin can mitigate asthma exacerbation induced by PM2.5 exposure.
- To elucidate the underlying mechanisms of apigenin's action, including its effects on immune cell responses and inflammatory pathways.
Main Methods:
- Ovalbumin (OVA)-sensitized BALB/c mice were used to model asthma.
- Mice were treated with apigenin (20 mg/kg/day) and exposed to PM2.5 (100 μg/mouse).
- Airway hyper-responsiveness (AHR), inflammatory cell infiltration (eosinophils, neutrophils), cytokine levels (IL-4, IL-13, IL-17), IgE, and NF-κB expression were measured.
Main Results:
- PM2.5 exposure aggravated AHR and induced a mixed T helper (Th)2/IL-17 response in asthmatic mice.
- Apigenin treatment significantly reduced AHR, eosinophil and neutrophil infiltration in bronchoalveolar lavage fluid (BALF) and lung tissue.
- Apigenin decreased total serum IgE, Th2 cytokines (IL-4, IL-13), Th17 cytokine (IL-17), and down-regulated NF-κB p65 expression.
Conclusions:
- Apigenin demonstrates significant anti-allergic and anti-neutrophil inflammatory activity in a PM2.5-exposed murine asthma model.
- Apigenin's therapeutic effects may be mediated by modulating IL-17 responses and inhibiting NF-κB signaling.
- Apigenin shows promise as a potential therapeutic agent for preventing PM2.5-induced exacerbation of pre-existing asthma.
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