非那雄胺对前列腺增生组织中微血管密度调控的机制探讨

目的 探讨非那雄胺对前列腺增生症组织中微血管调节因子表达的影响及意义.方法 取正常前列腺(NP)5例,前列腺增生症服用非那雄胺者(BPH+Finas)10例,前列腺增生症未服用非那雄胺者(BPH)30例的前列腺组织标本,采用免疫组化检测微血管调节因子内皮生长抑素(endostatin)、血管生长抑素(angiostatin)、血管形成因子-2(an-giopoietin-2)及血管内皮生长因子(VEGF)的表达,图像分析系统测量表达强弱.结果 BPH组endostatin、angiostatin表达较NP组明显减弱,而BPH+Finas组表达较BPH组明显增强;BPH组VEGF表达较NP组明显增强,而BPH+Finas组表达较BPH组明显减弱.endostatin阳性细胞计数(个/10Hp)在NP、BPH、BPH+Finas 3组分别为(129.00±10.68)、(34.00±15.38)、(142.10±12.22);angiostatin阳性细胞计数(个/10Hp)分别为(151.00±21.64)、(54.63±28.93)、(162.30±21.81);VEGF(灰度值)分别为(139.38±8.90)、(83.81±25.73)、(108.094-7.77),以上3组测值NP组和BPH+Finas组与BPH组比较差异均有显著性意义(均P<0.01).angiopoietin-2阳性细胞计数(个/10Hp)分别为(16.40±2.19)、(15.03±2.82)、(13.90±3.00),差异无显著性意义.结论 微血管调节因子endostatin、angiostatin、VEGF作用于局部组织的微循环,可能在前列腺增生症的病理生理过程中起重要调节作用.非那雄胺通过影响局部组织微血管调节因子,而发挥抑制前列腺增生的作用.

Effect of Finasteride on Regulation of the Microvessels in Tissue of Benign Prostatic Hyperplasia

Objective To explore the effect of Finasteride on regulation of microvessel regulatory factors in tissue of benign prostatic hyperplasia(BPH). Methods Prostatic tissues from 5 cases of normal prostates,10 cases of BPH treated with Finasteride,and 30 cases of BPH not treated with Finasteride were included in this study. Immunohistochemistry and imagine analysis system were used to detect the expression of endostatin,angiostatin,angiopoietin-2 and VEGF in the prostatic tissues. Results The expression of endostatin in normal prostate(NP) , BPH + Finasteride and BPH groups was (129. 00± 10. 68), (34. 00± 15. 38)and (142. 10± 12. 22)(P<0. 01) ,that of angiostatin was (151. 00±21. 64), (54. 63±28. 93) and (162. 30±21. 81) (P <0. 01), that of angiopoietin-2 was (116. 40 ±2.19), (15. 03 ± 2. 82) and (13. 90 ±3. 00) (P>0. 05), and that of VEGF was (139. 38 + 8. 90),(83. 81 ±25. 73) and (108. 09±7. 77)(P<0. 01)respectively. The expression of endostatin and angiostatin was significantly lower in BPH group than in NP group or BPH + Finasteride group. The expression of VEGF was higher in BPH group than in NP group or BPH + Finasteride group. Conclusion Microvessel regulatory factors endostatin, angiostatin and VEGF play a role in the pathophysiological process of BPH through their effects on the microcirculation of the local tissue. Finasteride could inhibit the proliferation of prostate cells through modulating the local microvessel regulatory factors.