亚洲酸通过自发性高血压大鼠中的NRF2/HO-1和TGF-β1/SMADS信号通路抑制心脏纤维化。
摘要来源：
int int himopharmacol。 2019年6月26日； 74：105712。 EPUB 2019年6月26日。PMID： 31254954“> 31254954 Yu-Zhou Liu，Shuai teng
文章隶属关系：zhe meng
摘要：
目标： abyiatic Acid Aciatic Acid Aciatic Acid Aciatic Acid Aciatic Aciatic Aciactiac（aa），以抑制肺部和肝纤维的影响，同时还对fibris（fibris）进行了影响。 We aimed to investigate whether AA could inhibit overpressure-induced cardiac fibrosis in spontaneous hypertension rats (SHRs).
METHOD: SHRs were treated with AA (20 mg kg day) for 12 weeks and cultured cardiac fibroblasts (CFs) were treated with Ang II （10mol/l）体外。测量氧化应激的标记，并用Sirius红色染色评估心脏纤维化的程度。使用商业测定套件测量了超氧化物歧化酶（SOD），丙二醛（MDA），活性氧香料（ROS）和谷胱甘肽（GSH）的水平。检测到胶原膜。 The expression of relative protein and mRNA was measured by Western blot and real-time PCR, respectively.
RESULTS: AA reduced systolic blood pressure, attenuated myocardial hypertrophy, reduced college deposition and the expression of collagen I and III, connective tissue growth factor, and plasminogen activator inhibitor-1,在mRNA和蛋白水平中，抑制TGF-β1表达，SMAD2/3的磷酸化以及SMAD7表达的增加。 AA降低了丙二醛和活性氧香料，同时增加了超氧化物歧化酶和谷胱甘肽的活性，并伴随着核TR的升高核因素红细胞2相关因子2（NRF2）以及血红素加氧酶（HO-1）和NAD（P）H脱氢酶[Quinone] 1（quinone] 1（NQO-1）的表达）的ANSLESTO Moreover, pretreating CFs with siRNA for Smad7 or Nrf2 both partially reversed the inhibition of AA on Ang II-induced cardiac fibrosis.
CONCLUSION: AA attenuates pressure overload-induced cardiac fibrosis via enhancing of Nrf2/HO-1 and suppressing TGF-β1/Smads磷酸化。