Abstract
Korean Red ginseng (KRG), commonly used in traditional medicine, has anti-inflammatory, anti- oxidative, and anti-tumorigenic properties. Asian sand dust (ASD) is known to aggravate upper and lower airway inflammatory responses. BEAS-2B cells were exposed to ASD with or without KRG or ginsenoside Rg3. Mucin 5AC (MUC5AC), MUC5B, and MUC8 mRNA and protein expression levels were determined using quantitative RT-PCR and enzyme-linked immunosorbent assay. Nuclear factor kappa B (NF-κB), activator protein 1, and mitogen-activated protein kinase expression and activity were determined using western blot analysis. ASD induced MUC5AC, MUC5B, and MUC8 mRNA and protein expression in BEAS-2B cells, which was significantly inhibited by KRG and Rg3. Although ASD-induced mucin expression was associated with NF-κB and p38 mitogen-activated protein kinase (MAPK) activity, KRG and Rg3 significantly suppressed only ASD-induced NF-κB expression and activity. KRG and Rg3 inhibited ASD-induced mucin gene expression and protein production from bronchial epithelial cells. These results suggest that KRG and Rg3 have potential for treating mucus-producing airway inflammatory diseases.
Highlights
Asian sand dust (ASD), originating from sandstorms in the Gobi Desert and the Ocher Plateau, is inhaled and comes into contact with respiratory epithelial cells, thereby inducing neutrophilic or eosinophilic lung inflammation by stimulating the production of inflammatory mediators [1,2]
We investigated the effects of Korean Red ginseng (KRG) and ginsenoside Rg3 on ASD-induced mucin production in bronchial epithelial cells
This study demonstrates that KRG and Rg3 inhibit ASD-induced Mucin 5AC (MUC5AC), MUC5B, and MUC8 mRNA and protein expression through the inhibition of NF-κB expression and activation independent of P38 mitogen-activated protein kinase (MAPK)
Summary
Asian sand dust (ASD), originating from sandstorms in the Gobi Desert and the Ocher Plateau, is inhaled and comes into contact with respiratory epithelial cells, thereby inducing neutrophilic or eosinophilic lung inflammation by stimulating the production of inflammatory mediators [1,2]. ASD influences morbidity and mortality in inflammatory airway diseases by increasing mucin gene expression in upper and lower airway epithelial cells, which causes mucus production, aggravation of respiratory symptoms and severity [7,8]. Mucins comprise about 2% of mucus with MUC2, MUC4, MUC5AC, MUC5B, and MUC8 commonly found in airway mucosa. MUC5AC and MUC5B constitute an important component of secretory mucin in airway diseases and are the subjects of frequent study [9,10]. MUC8 mRNA and protein levels were increased in sinus mucosa in chronic rhinosinusitis and in lung of cystic fibrosis, but the physiological functions of MUC8 remain unclear [11,12]
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