Abstract
Gyeji-tang (GJT), a traditional herbal formula composed of five herbal medicines, is commonly used to treat the common cold, exogenous febrile disease, fever and headaches in Korea, China and Japan. Although various pharmacological activities of GJT have been reported in several studies, the effect of GJT water extract (GJTWE) on airway inflammation has not yet been investigated. This study aimed to evaluate the effects of GJTWE on airway inflammation-related factors using human bronchial epithelial BEAS-2B cells, and to identify the phytochemicals in GJTWE by ultra-performance liquid chromatography-diode array detector-tandem mass spectrometry (UPLC-DAD-MS/MS) analysis. GJTWE significantly decreased the production of chemokines, including eotaxin-3, eotaxin-1, regulated on activation normal T-cell expressed and secreted (RANTES), and matrix metalloproteinase-9, and the expression of the adhesion molecules, intercellular adhesion molecule-1 and vascular cell adhesion molecule-1, in interleukin-4 + tumor necrosis factor-α (IT)-stimulated BEAS-2B cells. In the UPLC-DAD-MS/MS analysis, 21 phytochemicals, including six flavonoids, two chalcones, five terpenoids, six phenolics, one phenylpropanoid and one coumarin, were identified in GJTWE. The findings suggested that GJTWE might exhibit anti-inflammatory effects on airway inflammation by regulating the expression of inflammatory response-related factors in IT-stimulated BEAS-2B cells; further studies are required to determine the bioactive compounds involved in the inhibition of airway inflammation.
Highlights
Airway inflammation is an important factor in the pathogenesis of obstructive airway diseases, such as asthma and chronic obstructive pulmonary disease [1]
The human bronchial epithelial BEAS-2B cells stimulated by interleukin (IL)-4, tumor necrosis factor (TNF)-α, or lipopolysaccharide have been reported to secrete chemokines and cytokines such as eotaxin-1, eotaxin-3, regulated on activation normal T-cells expressed and secreted (RANTES), and IL-8, which contribute to airway inflammation [4,5,6]
Chemokines from bronchial epithelial cells have been reported to chronic airway inflammation by recruiting inflammatory cells
Summary
Airway inflammation is an important factor in the pathogenesis of obstructive airway diseases, such as asthma and chronic obstructive pulmonary disease [1]. The inflammatory response of the airway epithelium, mediated by the increased expression of chemokines, cytokines, inflammatory enzymes, and adhesion molecules, involves the recruitment, activation, and infiltration of inflammatory cells, along with the tissue remodeling of airways [1,2]. The human bronchial epithelial BEAS-2B cells stimulated by interleukin (IL)-4, tumor necrosis factor (TNF)-α, or lipopolysaccharide have been reported to secrete chemokines and cytokines such as eotaxin-1, eotaxin-3, regulated on activation normal T-cells expressed and secreted (RANTES), and IL-8, which contribute to airway inflammation [4,5,6]. The accumulation of leukocytes in the inflamed sites of the airways is a hallmark of asthma, and the infiltration of inflammatory cells occurs through the expression of adhesive molecules that regulate the adhesion of leukocytes and epithelial cells [7].
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