目的：观察糖肾方对糖尿病肾病大鼠模型足细胞蛋白 Desmin 的影响，通过以方测证的方法探讨足细胞损伤的中医病机。方法清洁级 SD 大鼠30只，予腹腔注射 STZ，制备糖尿病肾病（DN）大鼠模型，随机分为正常组、模型组、糖肾方组，正常组与模型组予蒸馏水灌胃，糖肾方组以糖肾方灌胃，6周后处死，收集血、尿液，检测血糖、尿微量白蛋白，光镜观察肾组织病理形态，RT-PCR 检测 Desmin 的 mRNA 表达。结果3组尿微量蛋白水平比较，糖肾方组大鼠尿微量蛋白（9.98±1.78）mg /24 h 少于模型组（14.64±2.73）mg /24 h（P ＜0.01）。光镜下观测肾小球病理改变发现，糖肾方组肾小球基底膜增厚，系膜基质增生等病理损伤程度均低于模型组。RT-PCR 显示糖肾方组 Desmin 表达（1.805±0.269）则明显低于模型组（3.548±0.621）（P ＜0.01）。结论糖肾方能够有效减少糖尿病肾病大鼠的蛋白尿，改善肾小球病理损伤，下调足细胞 Desmin 蛋白的表达，保护足细胞，并根据以方测证的原理推论虚和瘀可能是糖尿病肾病足细胞损伤的中医病机。%Objective To observe the effect of the diabetic nephropathy rats on the Desmin of the diabetic ne-phropathy rats. Methods Clean grade SD 30 rats,by intraperitoneal injection of STZ prepared diabetic nephropathy (DN)rat model,were randomly assigned to normal group,model group,Tangshenfang group,the normal group and model group received distilled water by gavage,Tangshenfang group take Tangshenfang orally,were killed after 6 weeks,collection of blood,urine,blood glucose,urinary albumin were observed with light microscope pathological mor-phology of the kidney tissue,and RT-PCR for detection of desmin mRNA expression. Results Three groups of urine protein and blood glucose levels,the urine of the Kidney Decoction group of rats with urine(9. 98 ± 1. 78)mg / 24 h less than the model group(14. 64 ± 2. 73)mg / 24 h(P < 0. 01). The pathological changes of the glomerular basement membrane were observed by light microscope,and the pathological damage of the glomerular basement membrane in the glucose and renal capsule group was lower than that in the model group. RT-PCR showed that the expression of Desmin in the diabetic group was significantly(1. 805 ± 0. 269)lower than that in the model group(3. 548 ± 0. 621) (P < 0. 01). Conclusion Tangshenfang can effectively reduce proteinuria in diabetic nephropathy rats,improve glo-merular injury and down regulated the expression of podocyte desmin protein,protect podocytes,and according to the measured in square card principle inference deficiency and blood stasis may is the Chinese medicine pathogenesis of podocyte injury in diabetic nephropathy.
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