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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
Author(s) -
Wanderley Maria I.,
Saraiva Karina L. A.,
César Vieira Juliany S. B.,
Peixoto Christina A.,
Udrisar Daniel P.
Publication year - 2013
Publication title -
international journal of experimental pathology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.671
H-Index - 72
eISSN - 1365-2613
pISSN - 0959-9673
DOI - 10.1111/iep.12026
Subject(s) - endocrinology , medicine , testosterone (patch) , ginseng , dexamethasone , pregnenolone , leydig cell , cholesterol side chain cleavage enzyme , chemistry , biology , steroid , hormone , luteinizing hormone , cytochrome p450 , metabolism , alternative medicine , pathology
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.