【摘要】 目的 評價非那雄胺對良性前列腺增生（benign prostate hyperplasia，BPH）細胞外基質（extracellular matrixc，ECM）的影響，并探討其作用機制。 方法 2008年6月－2009年3月選擇具備手術指征的BPH患者20例，按入院順序隨機分為非那雄胺組和安慰劑組。服藥4周后，行經尿道前列腺切除術（transurethral resection prostate，TURP），留取組織標本。另取正常前列腺標本6例，用免疫組織化學法結合圖像分析系統研究正常組、安慰劑組和非那雄胺組前列腺組織纖維連接蛋白（FN）、膠原（CL）、基質金屬蛋白酶2（MMP-2）、金屬蛋白酶組織抑制因子2（TIMP-2）的陽性表達。 結果 安慰劑組前列腺組織的FN、CL的陽性表達較正常組增強（P lt;0.01），MMP-2/TIMP-2差異無統計學意義（P gt;0.05）；非那雄胺組與安慰劑組相比，FN、CL的陽性表達減弱（P lt;0.01），而MMP-2/TIMP-2增高（P lt;0.01）。 結論 非那雄胺能降低BPH組織ECM成分，避免其沉積，其作用機制可能與其促進ECM降解有關。
【Abstract】 Objective To evaluate influence of finasteride on extracellular matrix (ECM) in benign prostate hyperplasia (BPH) patients and study the mechanism. Methods Twenty BPH patients needing surgery were randomly divided into 2 groups according to the sequence of hospitalization from June 2008 to March 2009. The finasteride group and the placebo group had 10 patients each. Transurethral resection prostate (TURP) were performed and the specimens were collected after 4 weeks of drug administration. Moreover, 6 normal prostatic tissues were selected. Expressions of fibronectin (FN), collagen (CL), matrix metalloproteinase-2 (MMP-2) and tissue inhibitor of metalloproteinase-2 (TIMP-2) were studied in prostatic tissues in all groups (including the normal group) by immunohistochemistry and image analysis system. Results Expressions of FN and CL were significantly higher than those in the normal group (P lt;0.01), while expressions of MMP-2 and TIMP-2 were not significantly different between them (P gt;0.05). Compared with the placebo group, expressions of FN and CL in the finateride group were significantly lower than the placebo group (P lt;0.01), while expressions of MMP-2 and TIMP-2 were significantly higher (P lt;0.01). Conclusions BPH is related to ECM depositing. Finasteride can decrease ECM of BPH and refrain it from depositing. Possibly, the principle is that finasteride can promote the degradation of ECM.
引用本文： 邵繼春,聶明,王林,張蜀武. 非那雄胺對增生前列腺組織細胞外基質的影響. 華西醫學, 2011, 26(7): 1054-1058. doi: 復制