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作 者:吴椋冰[1,2] 潘毅[2] 阳涛[3] 王志国[2] 钟婷[2] 李建平[2]
机构地区:[1]广西中医药大学,南宁530001 [2]广州中医药大学,广州510405 [3]萍乡市人民医院,江西萍乡337000
出 处:《中国实验方剂学杂志》2015年第14期92-96,共5页Chinese Journal of Experimental Traditional Medical Formulae
基 金:国家自然科学基金项目(81173181)
摘 要:目的:探讨"调肝肾,祛痰瘀"复方血压峰值前给药对自发性高血压大鼠(SHR)心肾组织转化生长因子-β1(TGF-β1)-Smads信号通路的影响。方法:将30只12周龄的自发性高血压大鼠,随机分为复方组(4 g·kg-1),氯沙坦组(30 mg·kg-1)和模型组,另设SD大鼠10只为正常组,12周后,采用RT-q PCR检测心肾组织Smad2,Smad3和Smad7 m RNA表达,免疫组化法检测肾组织Smad2,Smad3和Smad7蛋白表达。结果:与正常组比较,模型组肾脏Smad2,Smad3和心脏TGF-β1,Smad2,Smad3的m RNA表达明显升高,心脏和肾脏Smad7的m RNA表达明显降低(P<0.01),肾组织Smad2和Smad3的蛋白表达均明显升高,Smad7蛋白表达明显降低(P<0.01);与模型组比较,复方组能够下调肾脏Smad2,Smad3和心脏TGF-β1,Smad3的m RNA表达,上调肾脏和心脏Smad7的m RNA表达;复方组转化生长因子β1(TGF-β1)m RNA表达的下调程度比氯沙坦组明显(P<0.05);同时复方组的Smad2和Smad3的蛋白表达均明显下调(P<0.01),Smad7蛋白表达均明显上调(P<0.01),其中,复方组的Smad7蛋白表达与正常组无统计学差异。结论:调肝肾祛痰复方血压峰值前给药能够明显减少ECM聚积而减少高血压心肾纤维化。其作用机制应是在中医阴阳升降机制协同下,通过下调心肾的Smad2,Smad3和上调Smad7的表达以阻断TGF-β1-Smads信号转导通路所致。Objective: To observe the effect of Tiaoganshen Qutanyu-formula (TQF) on the pathway of transforming growth factor-β1 (TGF-β1) -Smad2/3/7 in the kidney of spontaneous hypertensive rats (SHR) administered before blood pressure peak. Method: A total of 30 12-week male SHR were randomly divided into 3 groups: the TQF group (4 g ·kg-1), the losartan group (30 mg·kg-1) and the normal group. Another healthy 10 SD rats were taken as the normal group. The mRNA expressions of Smad2, Smad3 and Smad7 in the heart and kidney were detected by RT-PCR, and the protein expressions of Smad2, Smad3 and Smad7 in the kidney were determined by munohistochemical method after 12 weeks of treatment. Result: Compared with the normal group, the mRNA expressions of Smad2, Smad3 in the kidney and TGF-β1 , Smad2, Smad3 in the heart increased, the mRNA expression of Smad7 in both kidney and heart decreased, the protein expressions of Smad2, Smad3 in the kidney increased, the protein expression of Smad7 decreased in the model group ( P 〈 0.01 ). Compared with model group, the mRNA expressions of Smad2, Smad3 in the kidney and TGF-fiI, Smad2, Smad3 in the heart decreased, the mRNA expression of Smad7 in both kidney and heart increased, the protein expressions of Smad2, Smad3 in the kidney decreased in the TQF group (P 〈 0. 05, P 〈 0.01 ). There was no statistical difference for protein expression of Smad7 between the TQF group and the normal group. Conclusion: TQF taken before blood pressure peak could reduce the hypertensive heart and kidney fibrosis by decreasing the aggregation of extra cellular matrix. The mechanism might be the synergistic effect of Yin-yang theory of the TGF-fl^-Smads signal pathway interruption by regulating the Smad2, Smad3 and Smad7 in the heart and kidney tissue.
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