Korean J Physiol Pharmacol.
2006 Oct;10(5):251-254.
Inhibition of Adenosine Triphosphate-stimulated Mucin Secretion from Airway Epithelial Cells by Schizandrin
- Affiliations
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- 1Department of Pharmacology, College of Medicine, Chungnam National University, Daejeon 301-131, Korea. LCJ123@cnu.ac.kr
- 2Department of Pharmacy, College of Pharmacy, Chungnam National University, Daejeon 301-131, Korea.
- 3Department of Pharmaceutical Sciences, College of Pharmacy, Seoul National University, Seoul 151-742, Korea.
- 4Department of Oriental Medicine, College of Oriental Medicine, Daejeon University, Daejeon 301-131, Korea.
- 5Department of Oriental Medicine, College of Oriental Medicine, Dongguk University, Gyeongju 780-714, Korea.
Abstract
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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.