加味当归补血汤通过调控TGF-β_1/Smad/ILK的表达对阿霉素肾病大鼠足细胞的保护作用

Protection mechanisms of Jiawei Danggui Buxue Decoction for podocytes in adriamycin-induced nephropathy rats by TGF-β_1/Smad/ILK cell signaling pathway

目的探讨应用加味当归补血汤对阿霉素肾病模型大鼠足细胞功能保护作用的机制。方法根据随机数字表法将32只SD大鼠随机分为空白组、模型组、洛汀新组、加味当归补血汤组。分别于造模前和造模后第1、3、5、7周检测24 h尿蛋白定量,实验结束时取肾组织进行光镜、免疫组化检测,用RT-PCR、Wetern blot方法对TGF-β1、ILK等蛋白表达的情况进行分析。结果加味当归补血汤可以明显减少尿蛋白的漏出,而病理学和分子生物学结果均提示加味当归补血汤组、洛汀新组对TGF-β1、ILK的表达具有调控作用,并与肾病蛋白nephrin表达密切相关。组间比较,差异有统计学意义(P<0.05)。结论加味当归补血汤通过抑制TGF-β1/Smad/ILK信号通路对阿霉素肾病模型大鼠的足细胞有较好的保护作用。

AIM To explore the mechanisms of Jiawei Danggui Buxue Decoction（ JDBD） ＇s protective effect on podocytes in rats with adriamycin-induced nephropathy. METHODS Thirty-two SD rats were divided into four groups with random number table（ JDBD group,benazepril group,model group and control group）. The 24 h-urine samples were collected to examine the quantitative estimation of urinary albumin in the 1st,3rd,5thand 7th week. At the end of the experiment,the renal tissue was excised for the test of HE and immunohistochemical stain.Their expressions of TGF-β1,Smads and ILK were analyzed by RT-PCR and Western blot. RESULTS JDBD group and benazepril group could reduce the leaking of proteinuria. The pathology and molecular biology tests showed that JDBD group and benazepril group had regulation function on the expressions of TGF-β1,Smads and ILK. Those changes were closely related to the expression of nephrin in renal tissue. There were statistical differences when comparing among groups. CONCLUSION JDBD can protect podocytes in adriamycin-induced nephropathy rats through inhibiting the cell signaling pathway of TGF-β1/ Smad / ILK.