Abstract
Xia-Bai-San (XBS) is a traditional Chinese medicine that has been used clinically for centuries in Asian countries to treat some types of common cold and asthma-like diseases similar to infantile pneumonia and childhood bronchitis. In previous studies, XBS was found to suppress the inflammatory process induced in lungs of mice treated with lipopolysaccharide (LPS). Purpose The present study was undertaken to examine the effects of XBS on LPS-inducible production of inflammatory cytokines, up-regulation of intercellular cell adhesion molecule-1 (ICAM-1), and activation of nuclear factor NF-κB in cultured human lung cells. Principal results Extracts of four raw herbs ( Cortex mori, Cortex lycii, Radix glycyrrhizae, and Fructus oryzae) were used to prepare the decoction. XBS decreased the histological damage and up-regulation of ICAM-1 observed in lungs of mice treated with lipopolysaccharide (LPS). In cultured human pulmonary epithelial A549 cells, XBS and its components Morus alba and Glycyrrhiza uralensis suppressed the up-regulation of IL-8 and ICAM-1 in response to LPS. Production of TNF-α, IL-1β, IL-6 and IL-8 by LPS-treated human THP-1 monomyelocytes was also suppressed by XBS. A549 cells expressed ICAM-1 in response to medium from LPS-treated THP-1 cells; expression was decreased by XBS. The adhesion of THP-1 cells to LPS-treated A549 cells were inhibited in the presence of XBS. Activation of NF-κB by LPS in A549 cells was suppressed by XBS, Morus alba, and Glycyrrhiza uralensis through inhibition of IκB phosphorylation; the concentrations at which suppression occurred were identical to those at which production of inflammatory cytokines and up-regulation of ICAM-1 were inhibited. Major conclusions These findings support the hypothesis that XBS, Morus alba, and Glycyrrhiza uralensis inhibit the inflammatory process in lung tissue through suppression of the IκB signaling pathway. XBS may prove helpful in the management of asthma, various allergic disorders, sepsis, or any other condition associated with pulmonary inflammation.
Published Version
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