Abstract
We demonstrate the mechanism by which Cordyceps sinensis (CS) mycelium regulates Leydig cell steroidogenesis. Mouse Leydig cells were treated with forskolin, H89, phorbol 12-myristate 13-acetate, staurosporine, or steroidogenic enzyme precursors with or without 3 mg/ml CS; then testosterone production was determined. H89, but not phorbol 12-myristate 13-acetate or staurosporine, decreased CS-treated Leydig cell steroidogenesis. CS inhibited Leydig cell steroidogenesis by suppressing the activity of P450scc enzyme, but not 3beta-hydroxysteroid dehydrogenase, 17alpha-hydroxylase, 20alpha-hydroxylase, or 17beta-hydroxysteroid dehydrogenase enzymes. Thus, CS activated the cAMP-protein kinase A signal pathway, but not protein kinase C, and attenuated P45scc enzyme activity to reduce human chorionic gonadotropin-stimulated steroidogenesis in purified mouse Leydig cells.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Androstenedione / metabolism
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Animals
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Cells, Cultured
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Colforsin / pharmacology
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Cordyceps / physiology*
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Cyclic AMP-Dependent Protein Kinases / antagonists & inhibitors
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Enzyme Inhibitors / pharmacology
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Hydroxycholesterols / pharmacology
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Isoquinolines / pharmacology
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Leydig Cells / drug effects
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Leydig Cells / enzymology
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Leydig Cells / metabolism*
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Male
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Mice
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Mice, Inbred C57BL
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Mycelium / physiology
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Progestins / metabolism
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Protein Kinase C / antagonists & inhibitors
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Staurosporine / pharmacology
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Sulfonamides*
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Testosterone / biosynthesis*
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Tetradecanoylphorbol Acetate / pharmacology
Substances
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Enzyme Inhibitors
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Hydroxycholesterols
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Isoquinolines
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Progestins
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Sulfonamides
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22-hydroxycholesterol
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Colforsin
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Testosterone
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Androstenedione
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Cyclic AMP-Dependent Protein Kinases
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Protein Kinase C
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Staurosporine
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N-(2-(4-bromocinnamylamino)ethyl)-5-isoquinolinesulfonamide
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Tetradecanoylphorbol Acetate