Regulatory mechanism of Cordyceps sinensis mycelium on mouse Leydig cell steroidogenesis

FEBS Letters

Hsu, Chih-Chao¹  Huang, Bu-Miin¹  Huang, Yuan-Li¹  Tsai, Shaw-Jeng² 

[1] Department of Cell Biology and Anatomy, College of Medicine, National Cheng Kung University, #1 Ta-Hsueh Road, Tainan 701, Taiwan;Department of Physiology, College of Medicine, National Cheng Kung University, #1 Ta-Hsueh Road, Tainan 701, Taiwan

关键词: Testosterone;    Mouse;    Leydig cell;    Steroidogenesis;    Cordyceps sinensis;    LH;    luteinizing hormone;    CS;    Cordyceps sinensis;    BSA;    bovine serum albumin;    PKA;    protein kinase A;    PKC;    protein kinase C;    3β-HSD;    3β-hydroxysteroid dehydrogenase;    17β-HSD;    17β-hydroxysteroid dehydrogenase;    H89;    N-(2-[p-bromocinnamylamino]ethyl)-5-isoquinolinesulfonamide hydrochloride;    PMA;    phorbol 12-myristate 13-acetate;   

DOI  :  10.1016/S0014-5793(03)00427-7

学科分类：生物化学/生物物理

来源: John Wiley & Sons Ltd.

【 摘 要 】

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.

【 授权许可】

Unknown