The prevalence of allergic asthma has increased markedly in recent decades and has become an important problem [
1]. Allergic asthma is caused mainly by allergens such as house dust, inhalants, foods, drugs, and animal dander and its symptoms include wheezing, coughing, tightness of the chest, and breathlessness [
2‐
4]. These symptoms results from bronchoconstriction and bronchial mucosal thickening caused by eosinophilic airway inflammation, airway remodeling, and excessive mucus production. Allergic asthma is regarded as a chronic inflammatory disease of the airway characterized by airway inflammation and is mucus hypersecretion [
5]. Airway inflammation in allergic asthma is under the control of complex regulatory mechanisms involving the releasing of T helper type 2 (Th2) cytokines, chemokines and other signaling molecules, including nitric oxide (NO) [
5,
6]. Under asthmatic condition, allergens processed by antigen-presenting cells induce the activation of Th2 cells, which release various cytokines, including interleukin (IL)-4, IL-5, and IL-13, which exacerbate the allergic response by increasing inflammatory cell infiltration into the airway and immunoglobulin (Ig)E secretion, and by stimulating mucus hypersecretion [
7,
8]. NO plays a crucial role in the pathogenesis of airway inflammation in allergic asthma. NO is synthesized from L-arginine by NO synthase (NOS), which exists in three isoforms: neuronal NOS (nNOS), endothelial NOS (eNOS), and inducible NOS (iNOS) [
6]. Both nNOS and eNOS are considered constitutive, and are involved in vasodilation and bronchodilation [
9]. iNOS seems to be involved mainly in immunomodulation [
6]. iNOS is stimulated by many proinflammatory cytokines, and is responsible for prolonged production of higher concentration of NO [
10]. iNOS production increases in asthmatic tissues and several types of inflammatory cells [
11]. Recent studies have also shown that reducing iNOS expression attenuates the asthmatic response in the respiratory tract in various asthma models [
10,
12,
13].
Currently, the standard medication for allergic asthma comprises combined therapy including inhaled corticosteroids, leukotriene receptor antagonists, and others [
14]. However, these drugs produce side effects and do not treat many asthmatic individuals consistently [
15]. There is a pressing need for new agents for treating allergic asthma, and herbal remedies are attracting increasing attention as potential agents for this condition. Many herbal remedies have shown protective effects in experimentally induced allergic asthma models [
16].
Dianthus superbus has long been used as a herbal medicine in Asia and as an anti-inflammatory agent in the treatment of urinary infections, carbuncles, and carcinoma of the esophagus [
17,
18]. A previous study reported on the antioxidant and cytotoxic activities of
D. superbus fructus ethanolic extract (DSE) [
19]. However, the effects of DSE have not been reported in a murine model of allergic asthma. The aim of this study was to investigate the effects of DSE on airway inflammation in a murine model of ovalbumin (OVA)-induce allergic asthma.