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Zhonghua Nan Ke Xue ; 11(6): 413-8, 2005 Jun.
Article in Chinese | MEDLINE | ID: mdl-15999482

ABSTRACT

OBJECTIVE: To study angiogenesis and regulatory factors in the proliferated prostatic tissues of Sprague Dawley (SD) rats with BPH induced by testosterone. METHODS: Sixteen castrated SD rats, aged 8 weeks and weighing 200 approximately 250 g, were equally randomized into a model group and a control group, and the BPH model was established by subcutaneous injection of testosterone. Immunohistochemistry and MIAS (micro-image analysis system) were used to test the manifestations of MVD (microvessel density), VEGF (vascular endothelium growth factor), flk-1, endostatin, MMP-2 (matrix metalloproteinase-2) and TIMP-2 (tissue inhibitor of metalloproteinase-2) in the prostatic tissues of both the model and the control groups. Multiple linear regression with the stepwise method was adopted to analyze the data. RESULTS: The manifestations of MVD, VEGF, flk-1, MMP-2, MMP-2/TIMP-2 and VEGF/endostatin in the model group were higher, while that of endostatin was lower than in the control group (P < 0.01), and the manifestation of TIMP-2 showed no statistical difference between the two groups. The regression analysis indicated that MVD was positively correlated to VEGF, VEGF/endostatin and MMP-2/TIMP-2 (r = 0.974, 0.986, 0.982, P < 0.05) and negatively correlated to endostatin (r = - 0.975, P < 0.05) . CONCLUSION: Testosterone could induce BPH in SD rats by increasing MVD and promoting the multiplication of vascular endothelial cells after regradation of basement membrane.


Subject(s)
Neovascularization, Pathologic/chemically induced , Prostate/blood supply , Prostatic Hyperplasia/chemically induced , Testosterone , Animals , Disease Models, Animal , Endostatins/biosynthesis , Male , Matrix Metalloproteinase 2/biosynthesis , Neovascularization, Pathologic/metabolism , Prostate/metabolism , Prostatic Hyperplasia/metabolism , Random Allocation , Rats , Rats, Sprague-Dawley , Tissue Inhibitor of Metalloproteinase-2/biosynthesis , Vascular Endothelial Growth Factor A/biosynthesis , Vascular Endothelial Growth Factor Receptor-2/biosynthesis
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