A double-blind placebo controlled study was performed in 35 benign prostatic hypertrophy (BPH) patients never treated before. The patients were randomized into two groups, the 1st (18 cases) receiving Serenoa repens extract (160 mg. t.d.) for 3 months up to the day before the operation of transvesical adenomectomy and the 2nd (17 cases) receiving placebo. Steroid receptors were evaluated in the nuclear (n) and cytosolic (c) fraction using the saturation analysis technique (Scatchard analysis or single saturating dose assay) for androgen (AR) and estrogen (ER) receptors and the enzyme immunoassay (EIA) for ER and progesterone receptors (PgR). Scatchard analysis of ERc and ERn revealed the presence of two classes of binding sites, one with high-affinity low-capacity binding and the other with low-affinity highcapacity binding. In the untreated BPH group, ER were higher in the n than in the c fraction. ERn were positive in 14 cases and ERc in 12 of 17 cases. In the BPH group treated with S. repens extract on the contrary, ERn were negative for both binding classes in 17 cases and ERc in 6 of 18 cases. Using EIA, ERn and ERc were detected in all 15 samples examined, but in the treated group, ERn were significantly (p<0.01) lower than in the untreated group, whilst ERc remained almost unchanged. Similar results were obtained measuring PgR; the n fraction of the treated group prostatic samples was significantly (p<0.01) lower than that of the untreated group. Finally, the determination of ARc were almost the same in the two groups. In conclusion, these findings show that S. repens extract is able to inhibit the nuclear estrogen receptors in prostatic tissue samples of BPH patients. The results obtained with the Scatchard analysis or the single saturating-dose assay are confirmed by ER-EIA and by PgR-EIA representing a marker of the estrogenic activity. A possible explanation for these findings is that S. repens extract contains at least two fractions, one with antiandrogenic, the other with antiestrogenic effect, able to block the translocation of ERc to the nuclei by competition. It cannot be excluded, however, that the primary effect is antiestrogenic and that the inactivation of AR and PgR is secondary to ER blockade.
DeSilverio F, at al. Eur Urol 21:309-314; 1992