AIM: 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.METHOD: 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. RESULTS: 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 wetweight 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. CONCLUSION: 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.%目的：研究爱普列特是否通过诱导前列腺细胞凋亡来治疗前列腺良性增生.探讨以前列腺酸性磷酸酶作为前列腺萎缩标志的可行性.方法：光镜观察细胞形态变化.TUNEL法和琼脂糖凝胶电泳检测DNA断裂.测定前列腺酸性磷酸酶的活性.结果：去势和爱普列特均诱发前列腺细胞发生细胞凋亡.去势引发的细胞凋亡的程度大于爱普列特.爱普列特和去势均降低了前列腺湿重和DNA含量，升高了DNA浓度.最大或接近最大的抑制发生在给药后10天.爱普列特抑制了前列腺酸性磷酸酶的活性，其变化与给药或去势后前列腺湿重和DNA含量的变化一致.结论：爱普列特通过诱发前列腺细胞凋亡来治疗前列腺良性增生.前列腺酸性磷酸酶的活性可作为前列腺萎缩的标志.
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