Inhibition of Adenosine Triphosphate-stimulated Mucin Secretion from Airway Epithelial Cells by Schizandrin

Schizandrae Fructus has been used for controlling respiratory allergic or inflammatory diseases in folk medicine and their components, schizandrin, schizandrin-A and gomisin-A were reported to have diverse biological effects. In this study, we investigated whether schizandrin, schizandrin-A and gomisin-A affect adenosine triphosphate (ATP)-induced mucin secretion from cultured airway epithelial cells. Confluent primary hamster tracheal surface epithelial (HTSE) cells were metabolically radiolabeled using 3H-glucosamine for 24 h and chased for 30 min in the presence of varying concentrations of each agent to assess the effects on 3H-mucin secretion. The results were as follows: 1) schizandrin significantly inhibited ATP-induced mucin secretion; 2) However, schizandrin-A and gomisin-A did not affect ATP-induced mucin secretion, significantly. We conclude that schizandrin can inhibit ATP-induced mucin secretion by directly acting on airway mucin-secreting cells. Therefore, schizandrin should further be investigated for the possible use as mucoregulators in the treatment of inflammatory airway diseases.

Glycyrrhizin and Morroniside Stimulate Mucin Secretion from Cultured Airway Epithelial Cells

In this study, we investigated whether glycyrrhizin, prunetin and morroniside affect mucin secretion from cultured airway epithelial cells and compared the possible activities of these agents with the inhibitory action on mucin secretion by poly-L-lysine (PLL) and the stimulatory action by adenosine triphosphate (ATP). Confluent primary hamster tracheal surface epithelial (HTSE) cells were metabolically radiolabeled using (3)H-glucosamine for 24 h and chased for 30 min in the presence of varying concentrations of each agent to assess the effects on (3)H-mucin secretion. The results were as follows: 1) glycyrrhizin and morroniside increased basal mucin secretion from airway; 2) prunetin did not affect basal mucin secretion; 3) glycyrrhizin did not inhibit ATP-induced mucin secretion. We conclude that glycyrrhizin and morroniside can increase basal mucin secretion, by directly acting on airway mucin-secreting cells and suggest that two compounds be further investigated for the possible use as mild expectorants during the treatment of inflammatory airway diseases.

Effects of Ambroxol, S-carboxymethylcysteine, Dextromethorphan and Noscapine on Mucin Release from Airway Goblet Cells

In the present study, we investigated whether ambroxol, S-carboxymethyl-L-cysteine, dextromethorphan and noscapine affect mucin release from airway goblet cells. Confluent primary hamster tracheal surface epithelial cells were metabolically radiolabeled and chased for 30 min in the presence of varying concentrations of the above agents to assess the effects on 3H-mucin release. Noscapine stimulated mucin release during 30 min of treatment period in a dose-dependent manner. However, ambroxol, S-carboxymethyl-L-cysteine and dextromethorphan showed no significant effect on mucin release during 30 min of treatment period. We conclude that noscapine can affect mucin release by acting on airway mucin-secreting cells.

Effects of Sphingosine-1-phosphate, Furosemide and Indomethacin on Mucin Release from Airway Goblet Cells

In this study, we investigated whether sphingosine-1-phosphate, furosemide, and indomethacin affect mucin release from airway goblet cells. Confluent primary hamster tracheal surface epithelial cells were metabolically radiolabeled and chased for 30 min or 24 hr in the presence of varying concentrations of the above agents to assess the effects on 3H-mucin release. Sphingosine-1-phosphate stimulated mucin release during 30 min of treatment period in a dose-dependent manner. However, furosemide and indomethacin showed no effect on both basal and stimulated mucin release during 30 min or 24 hr of treatment period. We conclude that sphingosine-1-phosphate can affect mucin release by directly acting on airway mucin-secreting cells.