Department of Urology, Union Hospital of Fujian Medical University, Fuzhou, China.
Int J Urol. 2014 Feb;21(2):195-9. doi: 10.1111/iju.12210. Epub 2013 Jul 2.
5-α Reductase inhibitor can reduce the volume of benign prostatic hyperplasia by lowering benign prostatic hyperplasia level and consequently inducing epithelial cells apoptosis. The present study investigated whether autophagy and apoptosis of benign prostatic hyperplasia epithelial cells are influenced by low benign prostatic hyperplasia levels.
PWR-1E prostate epithelial cells transfected with GFP-LC3 plasmid were subjected to androgen deprivation conditions. Then the autophagic puncta were evaluated by fluorescence microscopy, and the cellular apoptosis rate was detected by 4, 6-diamidino-2-phenylindole staining after blocking of autophagic process by 3-methyladenine. Furthermore, autophagy status was also determined in hyperplasia prostate tissues from 5-α reductase inhibitor-treated patients by immunohistochemistry.
In the androgen deprivation medium, autophagic punta increased markedly in PWR-1E cells, and blockage of autophagy by 3-methyladenine significantly promoted PWR-1E cells' apoptosis rate. In vivo, the expression of LC3 protein (an important autophagic marker) in hyperplasia prostate tissue significantly increased after 5-α reductase inhibitor treatment. Meanwhile, the prostate-specific antigen, as an inner control, decreased.
5-α Reductase inhibitor treatment increases autophagy and possibly decreases the apoptosis of prostate epithelial cells.
5-α 还原酶抑制剂可通过降低良性前列腺增生水平，诱导上皮细胞凋亡，从而缩小良性前列腺增生的体积。本研究旨在探讨低水平良性前列腺增生是否会影响良性前列腺增生上皮细胞的自噬和凋亡。
将 GFP-LC3 质粒转染的 PWR-1E 前列腺上皮细胞置于去雄激素条件下。然后通过荧光显微镜评估自噬斑点，并用 3-甲基腺嘌呤阻断自噬过程后通过 4,6-二脒基-2-苯基吲哚染色检测细胞凋亡率。此外，还通过免疫组织化学法检测了 5-α 还原酶抑制剂治疗患者增生前列腺组织中的自噬状态。
在去雄激素培养基中，PWR-1E 细胞中的自噬斑点明显增加，用 3-甲基腺嘌呤阻断自噬可显著促进 PWR-1E 细胞的凋亡率。在体内，5-α 还原酶抑制剂治疗后增生前列腺组织中 LC3 蛋白（一种重要的自噬标志物）的表达显著增加，同时前列腺特异性抗原（作为内参）减少。
5-α 还原酶抑制剂治疗可增加前列腺上皮细胞的自噬，并可能减少其凋亡。
