梗阻性肾病中肾小管周围毛细血管损伤的实验研究  

Peritubular capillary injury in experimental obstructive uropathy

作　　者：樊彩斌[1] 温端改[1] 侯建全[1] 郭震华[1] 周云[2] 严向明[2] 王兴东[2] 

机构地区：[1]苏州大学附属第一医院泌尿外科,215006 [2]苏州大学附属儿童医院泌尿外科

出　　处：《江苏医药》2008年第4期386-388,F0003,共4页Jiangsu Medical Journal

摘　　要：目的观察梗阻性肾病模型中肾小管周围毛细血管（PTC）损伤与肾小管上皮细胞凋亡的关系，并探讨血管内皮细胞生长因子（VEGF）对PTC的调节作用。方法建立SD大鼠单侧输尿管完全梗阻（CUUO）模型，用免疫组化方法检测PTC的密度和VEGF的表达水平，TUNEL法对PTC和肾小管上皮细胞进行原位凋亡测定，透射电镜观察超微结构变化。结果第7天VEGF染色局部增强，PTC数量变化不显著，肾小管上皮细胞凋亡很少见。第14-28天，VEGF表达逐渐下降，直至完全消失。PTC数量减少，肾小管扩张或萎缩明显。电镜显示肾小管上皮细胞、PTC内皮细胞死亡的主要形式为凋亡；TUNEL显示肾小管上皮细胞凋亡在第14天达到高峰，然后迅速下降。结论PTC减少是肾小管上皮细胞内VEGF表达不足引起的，在肾小管上皮细胞凋亡的过程中发挥了重要作用。Objective To explore the relationships between PTC regression and renal tubular cell apoptosis, and investigate PTC regulation by vascular endothelial growth factor （VEGF） during the course of experimental obstructive uropathy. Methods Complete unilateral ureteral obstruction was induced by ligation of the left ureter in SD rats. PTC density and the expression of VEGF and its receptor Flk-1 were detected immunohistochemically, and morphologic changes in PTC endothelial ceils and renal tubular epithetial ceils were examined using TUNEL technique and electrorr microscopic studies. Results On the 7th day, the irnmunohistochemical labeling of tubular VEGF was intensified, which was accompanied by deformation and dilation of PTC lumina, mild renal tubular cell apoptosis. On the 14 th day, the tubular VEGF labeling was reduced, and so were the Flk-1 labeled PTC numbers. By the 28 th day, the number of Flk-1-positive PTC lumina was significantly decreased in the areas of marked renal tubular atrophy. Conclusion Depletion of VEGF in renal tubular epithelial ceils is crucial to the loss of PTC, and PTC regression might contribute to renal tubular cell apoptosis.

关 键 词：梗阻性肾病 肾小管周围毛细血管 血管内皮细胞生长因子 凋亡 

分 类 号：R692[医药卫生—泌尿科学]