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非那雄胺通过诱导良性和恶性前列腺细胞凋亡并抑制其细胞黏附来靶向前列腺血管。

Finasteride targets prostate vascularity by inducing apoptosis and inhibiting cell adhesion of benign and malignant prostate cells.

作者信息

Sutton M Tandy, Yingling Melissa, Vyas Ash, Atiemo Humphrey, Borkowski Andrew, Jacobs Stephen C, Kyprianou Natasha

机构信息

Division of Urology, University of Kentucky Medical Center, 800 Rose Street, Lexington, KY 40536, USA.

出版信息

Prostate. 2006 Aug 1;66(11):1194-202. doi: 10.1002/pros.20444.

DOI:10.1002/pros.20444
PMID:16652387
Abstract

BACKGROUND

This study investigated the effects of finasteride, a 5alpha-reductase inhibitor, clinically used for the treatment of benign prostatic hyperplasia (BPH) on prostate tumor vascularity, apoptosis, and cell adhesion in situ and in vitro.

METHODS

Prostate specimens from BPH patients treated with finasteride for 1-12 months (n = 13), or without finasteride treatment (n = 14), were evaluated for apoptosis (TUNEL assay), microvessel density (Factor VIII), and prostate specific antigen (PSA) immunoreactivity. In vitro, the effect of finasteride was investigated in benign prostate cells, BPH-1, and its tumorigenic derivatives, CAFTD-01 and CAFTD-03, using Hoechst staining and cell adhesion assays.

RESULTS

A significant increase in the apoptotic index, and reduced microvessel density and PSA expression were detected in prostates from finasteride-treated patients, compared to controls (P < 0.01). In vitro finasteride led to a significant decrease in prostate epithelial cell adhesion (P < 0.05).

CONCLUSIONS

Finasteride can induce prostate apoptosis and reduce tissue vascularity by inhibiting epithelial cell adhesion. This evidence supports that finasteride has apoptotic and anti-angiogenic effects against benign and malignant prostate.

摘要

背景

本研究调查了临床上用于治疗良性前列腺增生(BPH)的5α-还原酶抑制剂非那雄胺对前列腺肿瘤血管生成、细胞凋亡及原位和体外细胞黏附的影响。

方法

对接受非那雄胺治疗1 - 12个月的BPH患者(n = 13)或未接受非那雄胺治疗的患者(n = 14)的前列腺标本进行细胞凋亡(TUNEL检测)、微血管密度(因子VIII)和前列腺特异性抗原(PSA)免疫反应性评估。在体外,使用Hoechst染色和细胞黏附试验研究非那雄胺对良性前列腺细胞BPH - 1及其致瘤衍生物CAFTD - 01和CAFTD - 03的影响。

结果

与对照组相比,在接受非那雄胺治疗患者的前列腺中检测到凋亡指数显著增加,微血管密度降低,PSA表达减少(P < 0.01)。在体外非那雄胺导致前列腺上皮细胞黏附显著降低(P < 0.05)。

结论

非那雄胺可通过抑制上皮细胞黏附诱导前列腺细胞凋亡并减少组织血管生成。这一证据支持非那雄胺对良性和恶性前列腺具有凋亡和抗血管生成作用。

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