부산대학교 도서관

Background: The actions of glucocorticoids in target tissues depend on the local metabolism of glucocorticoids catalyzed by 11ß-hydroxysteroid dehydrogenase (11ß-HSD) 1 and 2. Glucocorticoids are the most effective anti-inflammatory drugs in the treatment of nasal polyps. However, the mechanisms underlying the anti-inflammatory effects are unclear. Objective: The present study analyzed the expression of 11ß-HSD1, 11ß-HSD2, steroidogenic enzymes (CYP11B1, CYP11A1), in nasal polyp tissues, and endogenous cortisol levels in nasal polyp-derived epithelial cells. Methods: The expression levels and distribution pattern of 11ß-HSD1, 11ß-HSD2, CYP11B1, and CYP11A1 were determined in nasal polyp tissues or nasal polyp-derived epithelial cells using real-time PCR, Western blot, and immunohistochemistry. The expression levels of cortisol were determined in cultured polyp-derived epithelial cells treated with ACTH, 11ß HSD1 inhibitor, or siRNA technique. The effect of glucocorticoids on the expression levels of these enzymes was investigated in cultured cells. Results: 11ß-HSD1, 11ß-HSD2, CYP11B1, and CYP11A1 were expressed in nasal polyp tissues and nasal polyp-derived epithelial cells. Cortisol production in cultured epithelial cells was decreased in cells treated with 11ß-HSD1 siRNA or inhibitor, compared with non-treated cells. Cultured cells treated with ACTH induced increased cortisol production. 11ß-HSD1 expression levels were upregulated in cells treated with glucocorticoid. Conclusions: These results indicate that 11ß-HSD1 expressed in polyp-derived epithelial cells may be involved in anti-inflammatory function of glucocorticoid in treatment of nasal polyps, contributing to increased levels of endogenous cortisol.