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To evaluate the ability of epristeride to inhibit the prostatic glandular regrowth.Normal rats were castrated. Testosterone was injected to induce the regrowth of glandular cells. HE staining was performed. The height of the glandular epithelium and the acinar luminal areas were determined, and dihydrotestosterone (DHT) was detected by immunohistochemistry.Both the height and the acinar luminal areas were reduced by 48 % and 55 % in epristeride-treated group compared with control group respectively. The staining of DHT was comparatively strong in the control group. After 30-d of treatment, it turned much weaker.The regrowth of glandular cells was inhibited by epristeride via declining of the DHT concentration in the rat prostate.

To study molecular mechanism of epristeride in the treatment of benign prostatic hyperplasia and discuss the possibility of using prostate acid phosphatase (ACP) as a marker of the atrophy of prostatic gland in vivo.Morphological changes in cells were observed by light microscope. TdT-mediated dUTP-biotin nick end labeling (TUNEL) technique and agarose gel electrophoresis were performed to detect the nucleosomal DNA fragmentation. The activity of pACP was also assayed.Apoptosis occurred in both castration- and epristeride- treatment group. Both the degree and extent of apoptosis are much larger in the group of castration than that of epristeride-treated group. Both epristeride and castration decreased the prostate wet weight and DNA content but increased the prostate DNA concentration. Maximal or near maximal decreases were seen by d 10 in both groups. The activity of ACP was decreased by both castration and epristeride treatment. Changes in the ACP activity during treatment were coincide with other changes such as the prostate wet weight and DNA content.Apoptosis induced by epristeride was one of mechanisms in the treatment of benign prostatic hyperplasia and the activity of ACP could be used as a marker of prostate atrophy.

To study the effect of nomegestrol acetate, a new synthetic progesterone on granulosa cells' viability and steroidogenesis function.Granulosa cells were cultured in McCoy's 5A medium. Trypan blue stain was used to measure viable cells. FSH and testosterone were added to stimulate the steroid secretion. Specific RIA assay was used to evaluate the estrogen and progesterone secretion respectively.IC50 of nomegestrol acetate to damage cells is 6.85 mg/L (95 % confidence limits 5.36-8.75 mg/L). Nomegestrol acetate 0.45, 0.9, and 1.8 mg/L greatly inhibited the estrogen secretion from granulosa cells by 7.6 %, 12.5 %, 28.3 % in the presence of testosterone 0.5 micromol/L and FSH 10 U/L without affecting the number of viable cells. The secretion of progesteron were markedly decreased by 44.5 %, 53.3 %, and 62.0 % concurrently.Nomegestrol acetate directly inhibited the steroidogenesis of granulosa cells.