Foetal exposure to P anax ginseng extract reverts the effects of prenatal dexamethasone in the synthesis of testosterone by L eydig cells of the adult rat

Summary The aim of this study was to examine the effect of maternal exposure to P anax ginseng extract ( GE ) on the prenatal dexamethasone ( DEXA )‐induced increase in testosterone production by isolated L eydig 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 (dbc AMP ) or substrates of steroidogenesis [22( R )‐hydroxycholesterol (22( R )‐ OH ‐ C )] and pregnenolone. The capacity of rat L eydig cells exposed to DEXA to synthesize testosterone induced by dbc AMP , 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 L eydig 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. S t AR immunoexpression in Leydig cells was not modified by prenatal exposure to DEXA , GE or DEXA  +  GE . P 450scc 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 L eydig cells.