中文摘要：

目的观察祛风通络方对阿霉素肾病大鼠肾小球基底膜（GBM）上阴离子位点（AS）的影响。方法尾静脉注射阿霉素建立阿霉素肾病（AN）大鼠模型,并随机分为A（空白组）、B（模型组）、C（祛风通络方组）、D（激素＋祛风通络方组）、E（激素组）、F（苯那普利组）组,并给予相应干预;第3、7周留取肾皮质,以醋酸铀和柠檬酸铅双重染色法,透射电镜观察GBM的超微结构;以PEI示踪染色电镜观察GBM上AS的分布变化。结果①3周时与A组相比,模型组大鼠24 h尿蛋白显著升高（P〈0.01）,血清ALB明显下降（P〈0.01）,血清TG和TCH明显升高（P〈0.01）;②3周时透射电镜示模型组大鼠肾小球足突呈部分或弥漫性融合,GBM上AS明显减少;③7周时与B组相比,C、E组超微结构明显改善,AS分布呈连续点线状分布,平均AS表达量增强（P〈0.01）。结论祛风通络方可通过改善GBM上AS的表达与分布而修复肾小球电荷屏障。

英文摘要：

Objective To investigate the expression of anionic site in adriamycin-induced nephropathy （AN） rats, and to further explore the effects of Qufengtongluo Recipe on charge barrier in glomerulus in AN rats. Methods Adriamycin nephropathy was induced by a single tail intravenous injection of adriamycin. Totally 80 rats were randomly divided into normal control group and nephropathy model group. Three weeks later, the nephropathy model was established, and 50 AN rats were randomly divided into five groups： nephropathy model group （B, n = 10）, Qufeng group （C, n = 10）, prednisone and Qufeng group （D, n = 10）, prednisone group （E, n =10） and benazepri group （F, n = 10）, and they were treated respectively. With treatment being given respectively, renal tissue samples in each group were collected at week 3 and 7, respectively. The ultrastructure and expression of anionic site were examined by electron microscope observation. Results O After adriamycin injection, a significant increase of the 24-hour urinary protein was observed at week 3 （P〈0. 01）. In AN rats, serum albumin was decreased （P〈0.01） while serum TCH and TG were increased （P〈0.01）. （1） In AN rats the diffuse fusion and effacement of foot processes and decrease of anionic sites in GBM were observed at week 3. （2） At week 7, the average intensity of AS dramatically increased in C and E groups （P〈0.01） compared with that in nephropathy model group. Conclusion The abnormal expression of AS is the important mechanism that leads to the occurrence and development of proteinuria in AN rats. It is possible that Qufengtongluo Recipe has effects on nephrotic syndrome through altering the charge barrier in GBM in glomerulus.