Regulatory mechanism of Toona sinensis on mouse leydig cell steroidogenesis.
Toona sinensis (TS), a kind of arbor, widely distributes nowadays in Asia. The leaves of TS have been used as an effective nutritious food in Chinese society for a long time. It was reported that Toona sinensis can induce apoptosis of cancer cells, reduce plasma glucose in diabetic rats, and improve lipolysis of differentiated 3T3-L1 adipocyte and its uptake of glucose. It has also been shown that TS may increase dynamic activity of human sperm. Thus, we are interested to investigate whether Toona sinensis has any effect on mouse Leydig cell testosterone production, which correlates to sperm activity. Primary mouse Leydig cells were purified to conduct the in vitro experiments. Different concentrations of crude Toona sinensis were added to primary mouse Leydig cells and the testosterone production was determined. The results showed that crude TS significantly inhibited both basal and human chorionic gonadotropin (hCG)-stimulated testosterone productions in dose dependent manner, respectively (P<0.05). Crude TS also reduced the forskolin- and dibutyryl-cAMP (dbcAMP)-stimulated testosterone production (P<0.05), which indicated that crude TS might affect protein kinase A (PKA) signal transduction pathway at the site after the formation of cyclic AMP. Moreover, TS inhibited Leydig cell steroidogenesis by suppressing the activity of steroidogenic enzymes including P450 side chain cleavage enzyme, 3 beta-hydroxysteroid dehydrogenase, 17 alpha-hydroxylase, 20 alpha-hydroxylase and 17 beta-hydroxysteroid dehydrogenase (P<0.05). In summary, these results suggested that TS inhibited steroidogenesis by suppressing the cAMP-PKA signaling pathway and the activities of steroidogenic enzymes in normal mouse Leydig cells.
Poon
Song Ling
SL
Department of Cell Biology and Anatomy, College of Medicine, National Cheng Kung University, Tainan, 701 Taiwan, Republic of China.
Leu
Sew-Fen
SF
Hsu
Hseng-Kuang
HK
Liu
Ming-Yie
MY
Huang
Bu-Miin
BM
D019326:17-alpha-Hydroxyprogesterone / Q000494:pharmacology; D000735:Androstenedione / Q000494:pharmacology; D000818:Animals; D003994:Bucladesine / Q000494:pharmacology; D002478:Cells, Cultured; D006063:Chorionic Gonadotropin / Q000494:pharmacology; D005576:Colforsin / Q000494:pharmacology; D017868:Cyclic AMP-Dependent Protein Kinases / Q000378:metabolism; D003864:Depression, Chemical; D004305:Dose-Response Relationship, Drug; D006888:Hydroxycholesterols / Q000494:pharmacology; D007985:Leydig Cells / Q000187:drug effects / Q000378:metabolism*; D008297:Male; D029582:Meliaceae / Q000737:chemistry*; D051379:Mice; D008810:Mice, Inbred C57BL; D010936:Plant Extracts / Q000494:pharmacology; D018515:Plant Leaves / Q000737:chemistry; D011374:Progesterone / Q000494:pharmacology; D011863:Radioimmunoassay; D013256:Steroids / Q000096:biosynthesis*; D013268:Stimulation, Chemical; D013739:Testosterone / Q000096:biosynthesis
D006063:Chorionic Gonadotropin; D006888:Hydroxycholesterols; D010936:Plant Extracts; D013256:Steroids; C003585:22-hydroxycholesterol; D005576:Colforsin; D013739:Testosterone; D000735:Androstenedione; D011374:Progesterone; D003994:Bucladesine; D019326:17-alpha-Hydroxyprogesterone; D017868:Cyclic AMP-Dependent Protein Kinases