Abstract
Dipsacus asperoides C. Y. Cheng et T. M. Ai (DA) has been used in China as a traditional medicine to treat lumbar and knee pain, liver dysfunction, and fractures. We explored the suppressive effect of DA on allergic asthma using an ovalbumin (OVA)-induced asthma model. In the asthma model, female Balb/c mice were sensitized to OVA on day 0 and 14 to boost immune responses and then exposed to OVA solution by using an ultrasonic nebulizer on days 21 to 23. DA (20 and 40 mg/kg) was administered to mice by oral gavage on days 18 to 23. Methacholine responsiveness was determined on day 24 using a plethysmography. On day 25, we collected bronchoalveolar lavage fluid, serum, and lung tissue from animals under anesthesia. DA treatment effectively inhibited methacholine responsiveness, inflammatory cell infiltration, proinflammatory cytokines such as interleukin (IL)-5 and IL-13, and immunoglobulin (Ig) E in OVA-induced asthma model. Reductions in airway inflammation and mucus hypersecretion, accompanied by decreases in the expression of inducible nitric oxide synthase (iNOS) and the phosphorylation of nuclear factor kappa B (NF-κB), were also observed. Our results indicated that DA attenuated the asthmatic response, and that this attenuation was closely linked to NF-κB suppression. Thus, this study suggests that DA is a potential therapeutic for allergic asthma.
Highlights
Allergic asthma is a chronic inflammatory respiratory disease mediated by general environmental allergens and accompanied by symptoms such as wheezing, coughing, and airway remodeling [1]
The disease is featured as eosinophilic airway inflammation, mucus secretion, and airway hyperresponsiveness [2], and the development of the disease involves various cells, such as T-helper type 2 (Th2) cells, mast cells, and eosinophils [3]
nitric oxide (NO) has three isoforms: neuronal NOS, endothelial NOS, and inducible NOS [9]. iNOS is involved in the elevation of inflammatory cell infiltration into asthmatic lesions, which is stimulated by many pro-inflammatory cytokines [8]
Summary
Allergic asthma is a chronic inflammatory respiratory disease mediated by general environmental allergens and accompanied by symptoms such as wheezing, coughing, and airway remodeling [1]. The elevation in pro-inflammatory cytokines, including interleukin (IL)-4, IL-5, and IL-13, and the number of eosinophils are considered important factors in the pathogenesis of allergic asthma [4]. The increased expression of iNOS induces the elevation of NO production in patients with asthma and activates T-helper 2 lymphocytes [10,11]. These events eventually induce airway inflammatory responses via the elevation of inflammatory mediators. The activation of NF-κB, which is increased in the airways of patients with asthma and in asthmatic animals, induces the production of pro-inflammatory mediators. The downregulation of NF-κB may be a target for the treatment of allergic asthma
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