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pmid26045775
      Int+J+Clin+Exp+Pathol 2015 ; 8 (3 ): 2700-9
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  • Notoginsenoside R1 reduces blood pressure in spontaneously hypertensive rats through a long non-coding RNA AK094457 #MMPMID26045775
  • Yang Y ; Xi P ; Xie Y ; Zhao C ; Xu J ; Jiang J
  • Int J Clin Exp Pathol 2015[]; 8 (3 ): 2700-9 PMID26045775 show ga
  • Notoginsenoside R1 (NR1) is the main bioactive component in panaxnotoginseng, an old herb medicine widely used in Asian countries in the treatment of microcirculatory diseases. However, little is known about the effect of NR1 on antihypertension and the underlying mechanisms are still not clear. This study is aim to investigate the effect and elicit the mechanism of NR1 in antihypertension. Firstly, to assess the ability of NR1 in antihypertension, NR1 was injected in spontaneously hypertensive rats (SHR) via the vena caudalis. Then we examined the rats systolic blood pressure and inducible nitric oxide synthase (iNOS) activation in rats thoracoabdominal aortic. To further investigate the molecular mechanism of NR1 reduce blood pressure, primary SHR and WYK rat vascular endothelial cells (RVECs) were used for next study. LncRNAs related to hypertension were gained from bioinformatics analysis. The role of LncRNAs was finally characterized in RVECs by siRNA. Our results showed that NR1 significantly reduce blood pressure in SHR and induce nitric oxide (NO) generation through increasing the phosphorylation of iNOS. Through bioinformatics analysis and knockdown LncRNA AK094457 in RVECs, we also found LncRNA AK094457 promoted iNOS expression and NO concentration. Thus, we conclude that NR1 reduces the caudal blood pressure of SHR through induction of iNOS regulated by long non-coding RNA AK094457. These findings may have important implications for understanding the mechanisms of NR1 regulation blood pressure.
  • |Animals [MESH]
  • |Antihypertensive Agents/*pharmacology [MESH]
  • |Aorta/drug effects/enzymology/physiopathology [MESH]
  • |Blood Pressure/*drug effects [MESH]
  • |Cells, Cultured [MESH]
  • |Computational Biology [MESH]
  • |Disease Models, Animal [MESH]
  • |Endothelial Cells/drug effects/enzymology [MESH]
  • |Enzyme Activation [MESH]
  • |Gene Expression Profiling [MESH]
  • |Ginsenosides/*pharmacology [MESH]
  • |Hypertension/*drug therapy/enzymology/genetics/physiopathology [MESH]
  • |Male [MESH]
  • |Nitric Oxide Synthase Type II/genetics/metabolism [MESH]
  • |Nitric Oxide/metabolism [MESH]
  • |Phosphorylation [MESH]
  • |RNA Interference [MESH]
  • |RNA, Long Noncoding/*genetics [MESH]
  • |Rats, Inbred SHR [MESH]
  • |Rats, Inbred WKY [MESH]
  • |Time Factors [MESH]


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