Inhibition of Adenosine Triphosphate-stimulated Mucin Secretion from Airway Epithelial Cells by Schizandrin.
- Author:
Ho Jin HEO
1
;
Hyun Jae LEE
;
Cheolsu KIM
;
Ki Hwan BAE
;
Young Sik KIM
;
Sam Sik KANG
;
Yang Chun PARK
;
Yun Hee KIM
;
Un Kyo SEO
;
Jeong Ho SEOK
Author Information
1. Department of Pharmacology, College of Medicine, Chungnam National University, Daejeon 301-131, Korea. LCJ123@cnu.ac.kr
- Publication Type:Original Article
- Keywords:
Airway;
Mucin;
Schizandrin
- MeSH:
Adenosine Triphosphate;
Adenosine*;
Animals;
Cricetinae;
Epithelial Cells*;
Medicine, Traditional;
Mucins*;
Schisandra
- From:The Korean Journal of Physiology and Pharmacology
2006;10(5):251-254
- CountryRepublic of Korea
- Language:English
-
Abstract:
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.
