Direct effect of propylthiouracil on progesterone release in rat granulosa cells
| Autor: | Shyi-Wu Wang, Jiann-Jong Chen, Paulus S. Wang, Eileen-Jea Chien |
|---|---|
| Rok vydání: | 2003 |
| Předmět: |
Pharmacology
endocrine system medicine.medical_specialty Forskolin urogenital system Cholesterol side-chain cleavage enzyme Ovary Biology Calcium in biology Human chorionic gonadotropin chemistry.chemical_compound medicine.anatomical_structure Endocrinology chemistry Internal medicine medicine Pregnenolone Propylthiouracil Ovarian follicle hormones hormone substitutes and hormone antagonists medicine.drug |
| Zdroj: | British Journal of Pharmacology. 139:1564-1570 |
| ISSN: | 0007-1188 |
| DOI: | 10.1038/sj.bjp.0705392 |
| Popis: | The present study was to investigate the direct effect and action mechanism of propylthiouracil (PTU), an antithyroid drug, on the production of progesterone in rat granulosa cells. PTU (3–12 mM) decreased the basal and human chorionic gonadotropin (hCG)-stimulated release of progesterone from rat granulosa cells. PTU (3–12 mM) attenuated the stimulatory effects of forskolin and 8-bromo-cyclic 3′:5′-adenosine monophosphate on progesterone release from rat granulosa cells. PTU (12 mM) inhibited the activities of both the cytochrome P450 side-chain cleavage enzyme (P450scc, conversion of 25-hydroxyl cholesterol to pregnenolone) and the 3β-hydroxysteroid dehydrogenase (conversion of pregnenolone to progesterone) in rat granulosa cells. PTU decreased the Vmax but increased the Km of P450scc. PTU (12 mM) decreased the hCG-increased amount of steroidogenic acute regulatory (StAR) protein in rat granulosa cells. The present results suggest that PTU decreases the progesterone release by granulosa cells via a thyroid-independent mechanism involving the inhibition of post-cAMP pathway, and the activities of intracellular calcium, steroidogenic enzyme, and StAR protein functions. British Journal of Pharmacology (2003) 139, 1564–1570. doi:10.1038/sj.bjp.0705392 |
| Databáze: | OpenAIRE |
| Externí odkaz: |
|