补阳还五汤调节高血压前期大鼠肾脏肌成纤维细胞异常转化的机制研究

Mechanism of Tonifying Yang Decoction for Regulating Kidney Myofibroblasts Cells Abnormal Transformation of Prehypertension Rats

目的:通过观察补阳还五汤调节高血压前期大鼠肾脏TGF-β_1/Smads通路信号分子的表达作用,阐释补阳还五汤调节高血压前期大鼠肾脏肌成纤维细胞异常转化,延缓肾脏病理损伤的作用。方法:将20只雄性盐抵抗大鼠(dahl salt resistant rat,SS)随机分为正常对照组,中药对照组,20只雄性dahl盐敏感大鼠(dahl salt sensitive rat,DS)随机分为模型组和中药治疗组,每组10只。高盐饲料喂养12 d后,中药对照组和中药治疗组予以补阳还五汤灌胃治疗,每日1次,共治疗5周。治疗结束后取大鼠左肾组织检测TGF-β_1Smad2 Smad7及α-SMA的mRNA表达和P-Smad2蛋白表达。结果:与正常组比较,模型组TGF-β_1Smad2和α-SMA的mRNA表达升高(P<0.05),Smad7mRNA表达降低(P<0.05),P-Smad2蛋白表达升高(P<0.05);补阳还五汤治疗后,与模型组比较中药治疗组TGF-β_1Smad2和α-SMA的mRNA表达降低(P<0.05);Smad7mRNA表达升高(P<0.05),P-Smad2蛋白表达降低(P<0.05)。结论:补阳还五汤可能是通过调节肾脏TGF-β_1/Smads通路相关信号分子的表达抑制肌成纤维细胞异常转化,延缓肾脏病理损伤。

Objective： To explore effects of Tonifying Yang Decoction for recuperation of TGF-β_1/Smads pathway in kidney and reveal Tonifying Yang Decoction for regulating prehypertension rats kidney myofibroblasts cells abnormal transformation and delay the effect of renal pathological injury. Methods： Twenty male Dahl salt-resistant rats were randomly divided into the normal control group,the traditional Chinese medicine control group,each group 10. After 12 days＇ high salt feeding,continuous oral treatment of Tonifying Yang Decoction for recuperation,once a day,totally 5 weeks. After treatment,take out the left kidney and detect the expressions of TGF-β_1,Smad2,Smad7,α-SMA mRNA and the protein of P-Smad2. Results： Compared with the normal control group,the model group＇s expressions of TGF-β_1Smad2 and α-SMA mRNA increased（ P〈0. 05）. Smad7 mRNA reduced（ P〈0. 05）,P-Smad2 protein expression increased（ P〈0. 05）. After treatment of Tonifying Yang Decoction for recuperation,comparedwith the model group,Chinese medicine treatment group＇ s expressions of TGF-β_1Smad2 α-SMA mRNA reduced（ P〈0. 05）,Smad7 mRNA increased（ P〈0. 05） and P-Smad2 protein expression decreased（ P〈0. 05）. Conclusion： Tonifying Yang Decoction protects renal myofibroblasts cells abnormal transformation and delays renal pathological damage probably by changing the expression of TGF-β_1/ Smads pathway.