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目的:探讨血管新生(angiogenesis)及调控因子与睾酮刺激大鼠良性前列腺增生(BPH)的关系。方法:16只8周龄200~250gSD大鼠随机分为对照组与模型组各8只,采用去势后皮下注射丙酸睾酮法建立大鼠BPH模型。应用免疫组化结合图像分析系统检测对照组、BPH模型组前列腺组织微血管密度(MVD)、血管内皮生长因子(VEGF)、血管内皮生长因子受体1(flk-1)、内皮抑素(endostatin)、基质金属蛋白酶2(MMP-2)及其抑制剂(TIMP-2)的表达,并使用逐步引入剔除模型进行多元回归分析。结果:BPH模型组前列腺组织MVD明显增高(P<0.01),VEGF、flk-1、MMP-2的表达及MMP-2/TIMP-2、VEGF/endostatin比值均高于对照组(P<0.01),endostatin阳性表达低于对照组(P<0.01),TIMP-2表达与对照组比较差异无显著性。回归分析显示,MVD与VEGF、VEGF/endostatin、MMP-2/TIMP-2呈明显正相关(r=0.974、0.986、0.982,P均<0.05),与endostatin呈明显负相关(r=-0.975,P<0.05)。结论:雄激素致大鼠BPH与前列腺组织MVD增加有关,其MVD增加与血管基膜降解后血管内皮细胞增殖有关。
Objective: To investigate the relationship between angiogenesis and regulatory factors and testosterone-induced benign prostatic hyperplasia (BPH) in rats. Methods: Sixteen 8-week-old 200 ~ 250g SD rats were randomly divided into control group and model group, with 8 rats in each group. BPH model was established by subcutaneous injection of testosterone propionate. Immunohistochemistry and image analysis system were used to detect the expression of microvessel density (MVD), vascular endothelial growth factor (VEGF), flk-1, endostatin in BPH model group, , Matrix metalloproteinase 2 (MMP-2) and its inhibitor (TIMP-2) were detected by multiplex regression analysis. Results: The expression of VEGF, flk-1 and MMP-2 and the ratio of MMP-2 / TIMP-2 and VEGF / endostatin in BPH model group were significantly higher than those in control group (P <0.01) , the expression of endostatin was lower than that of the control group (P <0.01), while the expression of TIMP-2 was not significantly different from that of the control group. Regression analysis showed that there was a significant positive correlation between MVD and VEGF, VEGF / endostatin and MMP-2 / TIMP-2 (r = 0.974,0.986,0.982, P <0.05) P <0.05). Conclusion: Androgen-induced BPH is associated with an increase of MVD in prostate tissue, and its increased MVD is related to the proliferation of vascular endothelial cells after degradation of vascular basement membrane.