Total ginsenosides increase coronary perfusion flow in isolated rat hearts through activation of PI3K/Akt-eNOS signaling

Xiao Qin Yi, Ting Li, Jing Rong Wang, Vincent Kam Wai Wong, Pei Luo, Ivan Yuen Fan Wong, Zhi Hong Jiang, Liang Liu*, Hua Zhou

*Corresponding author for this work

Research output: Contribution to journalJournal articlepeer-review

39 Citations (Scopus)


Background: Ginseng is the most popular herb used for treatment of ischemic heart diseases in Chinese community; ginsenosides are considered to be the major active ingredients. However, whether ginsenosides can enhance the coronary artery flow of ischemic heart and, if so, by what mechanisms they do this, remains unclear. Methods: Isolated rat hearts with ischemia/reperfusion injury in Langendorff system were employed for examining the effect of total ginsenosides (TGS) on coronary perfusion flow (CPF). In addition, human aortic endothelial cells (HAECs) were used for mechanistic study. Levels of various vasodilative molecules, intracellular calcium concentration ([Ca2+]i), and expressions and activation of proteins involving regulation of nitric oxide (NO) signaling pathways in heart tissues and HAECs were determined. Results: TGS dose-dependently and significantly increased CPF and improved systolic and diastolic function of the ischemia/reperfused rat heart, while inhibitors of NO synthase (NOS), soluble guanylate cyclase (sGC), heme oxygenase (HO), cyclooxygenase (COX), and potassium channel abolished the vasodilation effect of TGS. Positive control verapamil was effective only in increasing CPF. TGS elevated levels of NO and 6-keto-prostaglandin F1α, a stable hydrolytic product of prostacyclin I2 (PGI2), in both coronary effluents and supernatants of HAECs culturing medium, and augmented [Ca2+]i in HAECs. TGS significantly up-regulated expression of phosphoinositide 3-kinase (PI3K) and phosphorylations of Akt and endothelial NOS (eNOS) as well. Conclusions: TGS significantly increased CPF of ischemia/reperfused rat hearts through elevation of NO production via activation of PI3K/Akt-eNOS signaling. In addition, PGI2, EDHF and CO pathways also partially participated in vasodilation induced by TGS.

Original languageEnglish
Pages (from-to)1006-1015
Number of pages10
Issue number13
Publication statusPublished - Nov 2010

Scopus Subject Areas

  • Molecular Medicine
  • Pharmacology
  • Pharmaceutical Science
  • Drug Discovery
  • Complementary and alternative medicine

User-Defined Keywords

  • Ginsenosides
  • Langendorff system
  • Myocardial ischemia/reperfusion injury
  • PI3K/Akt-eNOS signaling
  • Vasodilation


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