The regulatory mechanism of Tremella mesenterica on steroidogenesis in MA-10 mouse Leydig tumor cells

• Published in: Life sciences (1973) Vol. 79; no. 6; pp. 584 - 590
• Main Authors: Chen, Yen-Wen, Lo, Hui-Chen, Yang, Jyuer-Ger, Chien, Chi-Hsien, Lee, Shi-Hsiung, Tseng, Chi-Yu, Huang, Bu-Miin
• Format: Journal Article
• Language: English
• Published: Netherlands Elsevier Inc 04.07.2006
• Subjects: 3-Hydroxysteroid Dehydrogenases - metabolism; Animals; Basidiomycota; Cell Line, Tumor; Chorionic Gonadotropin - pharmacology; Colforsin - pharmacology; Cytochrome P-450 Enzyme System - metabolism; Leydig cell; Leydig Cell Tumor; Leydig Cells - drug effects; Leydig Cells - enzymology; Leydig Cells - metabolism; MA-10; Male; Medicine, Chinese Traditional; Mice; Phosphoproteins - biosynthesis; Progesterone; Progesterone - metabolism; Tremella mesenterica; Tremella mesenterica; MA-10; Progesterone; Leydig cell
• ISSN: 0024-3205; 1879-0631
• DOI: 10.1016/j.lfs.2006.02.003

Tremella mesenterica (TM), a yellow jelly mushroom, has been traditionally used as tonic food to improve body condition in Chinese society for a long time. We have previously demonstrated that TM reduced in vitro hCG-treated steroidogenesis in MA-10 mouse Leydig tumor cells without any toxicity effect. In the present study, the mechanism how TM suppressed hCG-treated steroidogenesis in MA-10 cells was investigated. MA-10 cells were treated with vehicle, human chorionic gonadotropin (hCG, 50 ng/ml), or different reagents with or without TM to clarify the effects. TM significantly suppressed progesterone production with the presences of forskolin (10 and 100 μM) or dbcAMP (0.5 and 1 mM), respectively, in MA-10 cells ( p < 0.05), which indicated that TM suppressed steroidogenesis after PKA activation along the signal pathway. Beyond our expectation, TM induced the expression of steroidogenic acute regulatory (StAR) protein with or without hCG treatments. However, TM profoundly decreased P450 side chain cleavage (P450scc) and 3β-hydroxysteroid dehydrogenase (3β-HSD) enzyme activities without any influences on the expression of both enzymes. These inhibitions on steroidogenic enzyme activities might counteract the stimulation of StAR protein expression. In conclusion, results suggest that TM suppressed hCG-treated steroidogenesis in MA-10 cells by inhibiting PKA signal pathway and steroidogenic enzyme activities.