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Regulatory mechanism of Cordyceps sinensis mycelium on mouse Leydig cell steroidogenesis
Author(s) -
Hsu Chih-Chao,
Tsai Shaw-Jeng,
Huang Yuan-Li,
Huang Bu-Miin
Publication year - 2003
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/s0014-5793(03)00427-7
Subject(s) - staurosporine , forskolin , leydig cell , protein kinase a , protein kinase c , cholesterol side chain cleavage enzyme , biology , enzyme , phorbol , endocrinology , biochemistry , microbiology and biotechnology , chemistry , medicine , hormone , receptor , luteinizing hormone , cytochrome p450
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 3β‐hydroxysteroid dehydrogenase, 17α‐hydroxylase, 20α‐hydroxylase, or 17β‐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.