Abstract
Asthma is a chronic respiratory disease mediated by airway inflammation. Jakyakgamcho-tang (JGT), a traditional medicine, is widely subscribed to common diseases such as muscle pain and cramps in East Asian countries. Although the efficacy of JGT on peripheral neuropathy, gouty arthritis, and colitis has been reported, the effect of JGT on airway inflammation related to asthma is not clearly investigated. In this study, we aimed to evaluate the effects of JGT water extract (JGTW) on factors related to airway inflammation using the human bronchial epithelial BEAS-2B and the mouse monocyte-macrophage RAW264.7 cell lines. Furthermore, the constituents in JGTW were quantitatively and qualitatively studied for future reference of JGTW standardization. JGTW reduced the generation of several airway inflammation mediators such as eotaxins, regulated on activation normal T-cell expressed and secreted (RANTES), and matrix metalloproteinase-9, and expressions of adhesion molecules (ICAM-1 and VCAM-1), which attracts leukocytes to the site of inflammation in interleukin-4 + tumor necrosis factor-α (IT)-stimulated BEAS-2B cells. In lipopolysaccharide-stimulated RAW264.7 cells, JGTW effectively suppressed inducible nitric oxide synthase (iNOS) induction by inhibiting the MAPK and NF-κB signaling. In addition, JGTW treatment showed decreased inflammatory cells and Th2 cytokines in bronchoalveolar lavage fluid and decreased IgE levels in plasma in the OVA-induced asthmatic mice model. In the ultra-performance liquid chromatography-diode array detector-tandem mass spectrometry analysis, 24 phytochemicals were identified in JGTW, and paeoniflorin (63.971 mg/g) and glycyrrhizin (11.853 mg/g) were found to be the most abundant. These findings suggest that JGTW has anti-inflammatory effects on airway inflammation by regulating inflammatory response-related factors, possibly through MAPK and NF-κB in pulmonary epithelial cells and macrophages.
Highlights
Asthma is a chronic respiratory disease known to be caused by excessive airway inflammation and hyper-responsiveness that leads to obstruction of airway [1]
Airway inflammation in asthma is induced by complex regulatory mechanisms involving the release of T helper 2 (Th2) cytokines (interleukin (IL)-4, IL-5, and IL-13), chemokines (eotaxins and regulated on activation, normal T-cell expressed and secreted (RANTES)), and other signaling molecules such as nitric oxide (NO) [2,3]
We explored the effect of JGT water extract (JGTW) on factors related to airway inflammation, a hallmark of asthma, in the human bronchial epithelial
Summary
Asthma is a chronic respiratory disease known to be caused by excessive airway inflammation and hyper-responsiveness that leads to obstruction of airway [1]. Airway inflammation in asthma is induced by complex regulatory mechanisms involving the release of T helper 2 (Th2) cytokines (interleukin (IL)-4, IL-5, and IL-13), chemokines (eotaxins and regulated on activation, normal T-cell expressed and secreted (RANTES)), and other signaling molecules such as nitric oxide (NO) [2,3]. Inflammatory cells, including eosinophil, mast cells and macrophages, contribute to the release of Th2 cytokines, chemokines, and tumor necrosis factor-α (TNF-α), a pro-inflammatory cytokine [4]. These soluble inflammatory mediators activate other proteins such as matrix metalloproteinase 9 (MMP-9), leading to degradation of the extracellular matrix, making respiratory microenvironment easier for inflammatory cells to infiltrate [5]. Overexpression of adhesion molecules, such as intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1
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