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National Journal of Andrology ; (12): 413-418, 2005.
Article Dans Chinois | WPRIM | ID: wpr-323347

Résumé

<p><b>OBJECTIVE</b>To study angiogenesis and regulatory factors in the proliferated prostatic tissues of Sprague Dawley (SD) rats with BPH induced by testosterone.</p><p><b>METHODS</b>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.</p><p><b>RESULTS</b>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) .</p><p><b>CONCLUSION</b>Testosterone could induce BPH in SD rats by increasing MVD and promoting the multiplication of vascular endothelial cells after regradation of basement membrane.</p>


Sujets)
Animaux , Mâle , Rats , Modèles animaux de maladie humaine , Endostatines , Matrix metalloproteinase 2 , Néovascularisation pathologique , Métabolisme , Prostate , Métabolisme , Hyperplasie de la prostate , Métabolisme , Répartition aléatoire , Rat Sprague-Dawley , Testostérone , Inhibiteur tissulaire de métalloprotéinase-2 , Facteur de croissance endothéliale vasculaire de type A , Récepteur-2 au facteur croissance endothéliale vasculaire
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