TargetRx Atlas

MRNA basic information

  • mRNA ID:ENST00000345060
  • Gene Name:ADRB3
  • mRNA database:Ensembl
  • mRNA expression :down-regulated
  • mRNA Method:RT-PCR
  • mRNA Pathway:NA
  • Evidence:validated
  • (mRNA-drug)

Drug basic information

  • Drug ID:NA
  • Drug Name:Si-Miao-Yong-An decoction
  • Drug Method:down-regulated the gene expression

Disease basic infommation

  • Disease:myocardial fibrosis
  • Tissue:patients tissues

Other information

  • Title:Dissection of mechanisms of Chinese medicinal formula Si-Miao-Yong-an decoction protects against cardiac hypertrophy and fibrosis in isoprenaline-induced heart failure
  • Journal:Journal of Ethnopharmacology
  • Published:2020
  • PubMed ID:31265887
  • Abstract:Aim of study:In this study, the potential mechanisms of SMYAD against cardiac fibrosis and hypertrophy in the β-adrenoceptor agonist isoprenaline induced heart failure model were investigated. Materials and methods:The heart failure animal model was established via injected isoprenaline in rats. Echocardiography was used to detect the structure and function of the heart. HE staining and Masson＇s trichrome staining was performed to assess myocardial tissue morphology. The serum biochemical indexes were detected by dedicated biochemical kit. BNP was tested by ELISA kit. The levels of mRNA were detected by RT-qPCR. Cardiomyocyte morphology was assessed by immunofluorescence. Phosphorylated and total p38, Akt were analyzed by Western blot. The production of reactive oxygen species (ROS) was tested by CM-H2DCFDA probe. Formula identification of chemical constituents of SMYAD in plasma was disclosed through ultra-performance liquid chromatography coupled to quadrupole time-of-flight mass spectrometry (UPLC-Q/TOF-MS). Results:SMYAD was able to improve the heart function in ISO induced heart failure rat model via protecting rat from developing cardiac hypertrophy and fibrosis. SMYAD also decreased plasma expression of these biochemical indexes. It was found that SMYAD could regulate cardiac hypertrophy and fibrosis makers＇ mRNA levels in vitro and vivo. In addition, SMYAD inhibited the phosphorylation of p38 and Akt, which are key mediators in the pathological process of ISO-induced cardiac hypertrophy and myocardial fibrosis. It also showed that the components of SMYAD in rat plasma exerted myocardial cell protective activity. Conclusion:In summary, SMYAD may comprise more than one active ingredient to the pursuit of combination therapies instead of specifically target a single disease-causing molecule. These experimental results suggest that SMYAD may be a potential drug candidate in diseases of cardiac hypertrophy and myocardial fibrosis caused by β-adrenoceptor abnormalities.
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