Foetal exposure to Panax ginseng extract reverts the effects of prenatal dexamethasone in the synthesis of testosterone by Leydig cells of the adult rat

• Published in: International journal of experimental pathology Vol. 94; no. 3; pp. 230 - 240
• Main Authors: Wanderley, Maria I., Saraiva, Karina L. A., César Vieira, Juliany S. B., Peixoto, Christina A., Udrisar, Daniel P.
• Format: Journal Article
• Language: English
• Published: England Blackwell Publishing Ltd 01-06-2013
• Subjects: Age Factors; Animals; Body Weight - drug effects; Cholesterol Side-Chain Cleavage Enzyme - metabolism; dexamethasone; Dexamethasone - pharmacology; Drug Interactions; Female; Glucocorticoids - pharmacology; leydig cells; Leydig Cells - metabolism; Leydig Cells - ultrastructure; Male; maternal exposure; Microscopy, Electron, Transmission; Organ Size - drug effects; Original; Panax - chemistry; Panax ginseng; Phosphoproteins - metabolism; Plant Extracts - pharmacology; Pregnancy; Prenatal Exposure Delayed Effects - metabolism; Rats; Rats, Wistar; Testis - cytology; Testis - drug effects; Testis - metabolism; testosterone; Testosterone - biosynthesis; Testosterone - blood
• ISSN: 0959-9673; 1365-2613
• DOI: 10.1111/iep.12026

Summary
The aim of this study was to examine the effect of maternal exposure to Panax ginseng extract (GE) on the prenatal dexamethasone (DEXA)‐induced increase in testosterone production by isolated Leydig cells in adult rats. Pregnant rats were treated with (i) GE (200 mg/kg) or vehicle on days 10–21; (ii) DEXA (100 μg/kg) or vehicle on days 14–21; or (iii) a combination of GE plus DEXA at the same doses and with the same regimen. Testosterone production was induced either by the activator of protein kinase A (dbcAMP) or substrates of steroidogenesis [22(R)‐hydroxycholesterol (22(R)‐OH‐C)] and pregnenolone. The capacity of rat Leydig cells exposed to DEXA to synthesize testosterone induced by dbcAMP, 22(R)‐OH‐C or pregnenolone was increased in comparison with the control group. Combined exposure to DEXA + GE prevented the effect of DEXA on the responsiveness of Leydig cells to all inductors of testosterone synthesis, whereas GE alone did not modify the response to inductors. No modifications in testosterone production were observed under basal conditions. StAR immunoexpression in Leydig cells was not modified by prenatal exposure to DEXA, GE or DEXA + GE. P450scc and glucocorticoid receptor immunoexpression was higher in offspring exposed to DEXA in comparison with the control group. This increased expression was prevented by combined treatment with DEXA + GE. The present findings demonstrate that GE is capable of reversing the effect of DEXA on testosterone synthesis by rat Leydig cells.