2-Undecanone alleviates asthma by inhibiting NF-κB pathway

Abstract

Asthma is characterized by airway inflammation and remodeling. 2-undecanone (methyl nonyl ketone), a volatile organic compound originating from Houttuynia cordata, has the potential to ameliorate inflammatory diseases. The present study aimed to explore potential benefits of 2-undecanone in asthma. 2-undecanone (100, 200 or 400 mg/kg) was administered intragastrically to ovalbumin (OVA)-challenged BALB/c mice. Lung tissues were collected to observe histopathological changes, and bronchoalveolar lavage fluid (BALF) was collected for inflammatory cells analysis and cytokine production. The results showed that 2-undecanone ameliorated OVA-induced pathologic changes of lungs, including reducing inflammatory cell infiltration, goblet cell hyperplasia, and airway smooth muscle thickness. The number of inflammatory cells and the levels of IL-4, IL-5, IL-13, and IgE in BALF were decreased by 2-undecanone in asthmatic mice. Furthermore, abnormal activation of NF-κB pathway in lung tissues of asthmatic mice was impeded by 2-undecanone. In vitro, 2-undecanone (12.5, 25, or 50 μM) suppressed platelet-derived growth factor-BB (PDGF-BB)-induced proliferation and migration of primary airway smooth muscle cells (ASMCs), and inhibited the switching of ASMCs from contractile phenotype to synthetic phenotype. Consistently, 2-undecanone blocked NF-κB activation in ASMCs. Collectively, 2-undecanone relieves asthma through alleviating airway inflammation and remodeling, and this beneficial effect is achieved by inhibiting NF-κB pathway.

Undaria pinnatifida ameliorates nasal inflammation by inhibiting eosinophil and mast cell activation and modulating the NF‐κB/MAPKs signaling pathway

“…47 Following translocation to the nucleus, NF-κB p65 undergo translation, leading to the synthesis of inflammatory mediators, including IL-6 and TNF-α, as well as Th2 cytokines (IL-4, IL-5, and IL-13) in the context of allergic airway inflammation. 48 Upon activation of pathogens via IgE-mediated responses, MAPKs, including p38, ERK, and JNK, are phosphorylated. The nuclear translocation of AP-1, which transcribes and generates cytokines, is facilitated by these MAPKs.…”

“…This causes IκBα to break down and NF‐κB p65 and p50 dimers to form 47 . Following translocation to the nucleus, NF‐κB p65 undergo translation, leading to the synthesis of inflammatory mediators, including IL‐6 and TNF‐α, as well as Th2 cytokines (IL‐4, IL‐5, and IL‐13) in the context of allergic airway inflammation 48 . Upon activation of pathogens via IgE‐mediated responses, MAPKs, including p38, ERK, and JNK, are phosphorylated.…”