Deguelin Attenuates Allergic Airway Inflammation via Inhibition of NF-κb Pathway in Mice

Abstract

Asthma is a chronic respiratory disease characterized by airway inflammation and remodeling, resulting in a substantial economic burden on both patients and society. Deguelin, a constituent of the Leguminosae family, exhibits anti-proliferative and anti-inflammatory activities in cancer mice models via inhibiting phosphatidylinositol 3-kinases and the NF-κB pathway. We demonstrated that deguelin effectively reduced OVA-induced inflammatory cell recruitment, decreased lung tissue inflammation and mucus production, suppressed airway hyperresponsiveness, and inhibited serum immunoglobulin and Th2 cytokine levels in a dose-dependent manner in asthmatic mice. In addition, we found that deguelin reduced inflammatory gene expressions both in vivo and in vitro, which were closely associated with activation of the NF-κB signaling pathway. Thus, we further explored the underlying mechanisms of deguelin in normal human bronchial epithelial cells (BEAS-2B). Our results suggested that deguelin inhibited NF-κB binding activity by enhancing the ability of IκBα to maintain NF-κB in an inactive form in the cytoplasm and preventing the TNF-α induced translocation of p65 to the nucleus. In conclusion, our research indicates that deguelin attenuates allergic airway inflammation via inhibition of NF-κB pathway in mice model and may act as a potential therapeutic agent for patients with allergic airway inflammation.

Chrysophanol attenuates airway inflammation and remodeling through nuclear factor‐kappa B signaling pathway in asthma

“…During the past few decades, a number of natural herbs have been used for the prevention and treatment of asthma (Bao et al, ; Cho et al, ; Chunlian et al, ). Chrysophanol (CHR), a member of the anthraquinone family, was originally extracted from Rheum palmatum L., and it has been shown to display multiple pharmacological effects, such as anti‐inflammation (S. J. Kim et al, ), antitumor (Ni et al, ), antivirus (Chang, Huang, Lin, Tsou, & Lin, ), and antiproliferation (Hu, Zhang, Meng, Wang, & Wang, ).…”

Therapeutic Effect of Dipsacus asperoides C. Y. Cheng et T. M. Ai in Ovalbumin-Induced Murine Model of Asthma

“…These events eventually induce airway inflammatory responses via the elevation of inflammatory mediators. In addition, NF-κB is a transcription factor and is considered as an important factor in the pathogenesis of asthma because its activation induces inflammatory and immune responses [12,13]. 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.…”

Banhahubak-Tang Tablet, a Standardized Medicine Attenuates Allergic Asthma via Inhibition of Janus Kinase 1 (JAK1)/ Signal Transducer and Activator of Transcription 6 (STAT6) Signal Pathway

“…IgG, which is a T-cell elicited antibody, is correlated with IgE levels [28]. Therefore, production level of IgE and IgG are important therapeutic marker to treat allergic asthma [28,29]. There was an increase on influx of inflammatory cells into the airway by allergen exposure, which is verified by elevation of total inflammatory cell counts in the OVA + PM group.…”

“…Th2-elicited cytokines, IL-4 and IL-13 is contributed to switch B-cell to inflammatory mediator, IgE, which is bound with mast cells that released histamine. IgG, which is a T-cell elicited antibody, is correlated with IgE levels [28]. Therefore, production level of IgE and IgG are important therapeutic marker to treat allergic asthma [28,29].…”