扶正化瘀方抗肾间质纤维化作用机理的研究

目的探讨扶正化瘀方影响转化生长因子p（TGF-β）1信号转导与肾小管上皮细胞转分化的抗氯化汞中毒大鼠肾间质纤维化的作用机理。方法SD雄性大鼠44只，随机分为正常组、模型组、扶正化瘀方组（FZHY组）与维生素E组（Vit．E组），以8mg／kg氯化汞水溶液灌胃9周制备大鼠肾间质纤维化模型。从造模开始扶正化瘀方组以扶正化瘀方4．6g／kg大鼠体重灌胃，Vit．E组以100mg，kg大鼠体重VitE水溶液灌胃，1次／天，共9周。免疫荧光法观察肾组织α-平滑肌肌动蛋白、E-cadherin、TGF-β1表达，Western blot观察肾组织α-平滑肌肌动蛋白、E-cadherin、TGF-β1、TβR-1、Smad2、P-Smad2蛋白表达。结果与正常组相比，模型组肾组织E-cadherin表达明显降低，扶正化瘀方干预后其表达明显升高；模型组α-SMA、TGF-β1、TBR—1、P—Smad2表达明显升高，扶正化瘀方干预能降低其表达。各组大鼠Smad2表达无明显差异。结论扶正化瘀方可抑制肾小管上皮细胞转分化从而减轻肾间质纤维化，其机制与抑制纤维化肾脏TGF-β及其Ⅰ型受体的表达、下调Smad2活性，抑制TGF—β／Smads病理信号转导有关。

Fuzheng huayu recipe counteracts TGF-β1 induced epithelial-to-mesenchymal transition and reverses renal interstitial fibrosis in rats induced by HgC12

Objective To investigate the effects of Fuzheng Huayu Recipe on renal interstitial fibrosis, and its action mechanism involving in regulating TGF-β1/Smads signal transduction and tubular epithelial-to mesenchymal transition （EMT）.Methods： The rats were randomly divided into 4 groups： normal group, model group, Fuzheng Huayu group （FZHY group） and VitE group. Renal interstitial fibrosis model was induced by administration of HgC12 at a dose of 8mg/kg rat weight once day for 9 weeks. Meanwhile rats in FZHY group and VitE group were treated with Fuzheng Huayu Decoction at a dose of 4.6g/kg rat weight, and VitE at a dose of 100mg/kg rat weight respectively once a day for 9 weeks. Protein expressions of TGF- β 1, TGF- β receptor I （T β R-1）, Smad2, p-Smad2 in liver were analyzed by Western Blot. Protein expression and location of α -SMA, E-cadherin and TGF β 1 were analyzed by immunofluorescent stain. Results Compared to model group, Fuzheng Huayu Recipe upregulated E-cadherin protein expression, down-regulated protein expression of α-SMA, TGF- β1, p-Smad2and T β R-I.Conclusion： Fuzheng Huayu Decoction could ameliorate renal interstitial fibrosis in rats induced by HgC12, which was related to inhibiting TGF-β/Smads signal transduction and inhibiting EMT.