Abstract
So-Cheong-Ryoung-Tang is a traditionally used herbal formula for the treatment of pulmonary diseases in China, Korea, and Japan. We investigated the protective effects of So-Cheong-Ryong-Tang water extract (SCWE) in cigarette smoke concentrate (CSC) stimulated human airway epithelial cell line NCI-H292 and mice exposed cigarette smoke (CS) and lipopolysaccharide (LPS). In the CSC-stimulated NCI-H292 cells, SCWE inhibited proinflammatory cytokines in a concentration-dependent manner, as evidenced by a reduction in their mRNA levels. Also, SCWE significant reduced inducible nitric oxide synthase (iNOS) expression and nuclear factor kappa B (NF-κB) phosphorylation in CSC-stimulated cells. The mice were exposed to CS for 1 h per day (a total of eight cigarettes per day) for 7 days and received LPS intranasally on day 5. The mice were administered a dose of SCWE (100 and 200 mg/kg) 1 h before CS exposure. In in vivo, SCWE decreased the inflammatory cell count and reduced the expression of the proinflammatory cytokines in the broncho-alveolar lavage fluid (BALF) compared with CS and LPS exposed mice. SCWE attenuated inflammatory cell infiltration in airway induced by CS and LPS exposure, and this decrease was accompanied by a reduction in the expression levels of iNOS and MMP-9 in lung tissue. The extract also inhibited the phosphorylation of inhibitor of kappa B alpha (IκBα) and NF-κB induced by CS and LPS exposure in lung tissue. These results suggest that SCWE may effectively inhibit airway inflammatory responses induced by CS and LPS exposure via the NF-κB pathway. Therefore, SCWE may be a potential treatment for airway inflammatory diseases, such as chronic obstructive pulmonary disease (COPD).
Highlights
Chronic obstructive pulmonary disease (COPD) is a chronic inflammatory disease of the airway
We evaluated the protective effects of So-Cheong-Ryong-Tang water extract (SCWE) on airway inflammation induced by cigarette smoke (CS) and LPS exposure
SCWE effectively decreased the enhanced expression of inducible nitric oxide synthase (iNOS) and phosphorylation of IκBα and NF-κB induced by CS and LPS exposure in lung tissue, which were accompanied by reductions in the inflammatory responses and matrix metalloproteinases (MMPs)-9 expression in lung tissue
Summary
Chronic obstructive pulmonary disease (COPD) is a chronic inflammatory disease of the airway. The pathology of COPD is characterized by neutrophilic airway inflammation, airway remodeling, and pulmonary emphysema in response to cigarette smoke (CS) exposure (Dong et al, 2015; Jung et al, 2016a). CS exposure leads to airway inflammation, enhanced levels of proinflammatory cytokines and chemokines, and airspace enlargement (Jung et al, 2016b). MMPs are involved in the development of COPD via modulation of cytokine and chemokine production, extracellular matrix turnover, and tissue remodeling (Cane et al, 2016). MMP-9 was found in the sputum and lavage samples of patients with COPD, and its expression was associated with activation of nuclear factor kappa B (NF-κB), resulting in inflammatory responses (Pang et al, 2015)
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