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Ginsenoside Rb1 protects against ischemia/reperfusion-induced myocardial injury via energy metabolism regulation mediated by RhoA signaling pathway.

Abstract
Cardiac ischemia and reperfusion (I/R) injury remains a challenge for clinicians. Ginsenoside Rb1 (Rb1) has been reported to have the ability to attenuate I/R injury, but its effect on energy metabolism during cardiac I/R and the underlying mechanism remain unknown. In this study, we detected the effect of Rb1 on rat myocardial blood flow, myocardial infarct size, cardiac function, velocity of venule red blood cell, myocardial structure and apoptosis, energy metabolism and change in RhoA signaling pathway during cardiac I/R injury. In addition, the binding affinity of RhoA to Rb1 was detected using surface plasmon resonance (SPR). Results showed that Rb1 treatment at 5 mg/kg/h protected all the cardiac injuries induced by I/R, including damaged myocardial structure, decrease in myocardial blood flow, impaired heart function and microcirculation, cardiomyocyte apoptosis, myocardial infarction and release of myocardial cTnI. Rb1 also inhibited the activation of RhoA signaling pathway and restored the production of ATP during cardiac I/R. Moreover, SPR assay showed that Rb1 was able to bind to RhoA in a dose-dependent manner. These results indicate that Rb1 may prevent I/R-induced cardiac injury by regulation of RhoA signaling pathway, and may serve as a potential regime to improve percutaneous coronary intervention outcome.
AuthorsYuan-Chen Cui, Chun-Shui Pan, Li Yan, Lin Li, Bai-He Hu, Xin Chang, Yu-Ying Liu, Jing-Yu Fan, Kai Sun, Quan -Li, Jing-Yan Han
JournalScientific reports (Sci Rep) Vol. 7 Pg. 44579 (03 22 2017) ISSN: 2045-2322 [Electronic] England
PMID28327605 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
Chemical References
  • Cardiotonic Agents
  • Ginsenosides
  • Troponin I
  • ginsenoside Rb1
  • Adenosine Triphosphate
  • RhoA protein, rat
  • rho GTP-Binding Proteins
Topics
  • Adenosine Triphosphate (agonists, biosynthesis)
  • Animals
  • Apoptosis (drug effects)
  • Blood Flow Velocity
  • Cardiotonic Agents (pharmacology)
  • Energy Metabolism (drug effects)
  • Gene Expression Regulation
  • Ginsenosides (pharmacology)
  • Heart Function Tests
  • Male
  • Myocardial Infarction (genetics, metabolism, pathology, prevention & control)
  • Myocardial Reperfusion Injury (genetics, metabolism, pathology, prevention & control)
  • Myocardium (metabolism, pathology)
  • Myocytes, Cardiac (drug effects, metabolism, pathology)
  • Protein Binding
  • Rats
  • Rats, Sprague-Dawley
  • Signal Transduction (drug effects)
  • Surface Plasmon Resonance
  • Troponin I (genetics, metabolism)
  • rho GTP-Binding Proteins (genetics, metabolism)

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