Ginsenoside Rb1 preconditioning protects against myocardial infarction after regional ischemia and reperfusion by activation of phosphatidylinositol-3-kinase signal transduction.
BACKGROUND
Ginsenoside Rb1, a major bioactive component of Panax ginseng, bears various beneficial effects on the cardiovascular system. This study investigated whether ginsenoside Rb1 preconditioning has protective effects on myocardial ischemia-reperfusion injury and its potential mechanism.


METHODS
Rats subjected to 45 min of myocardial ischemia followed by 120 min of reperfusion were assigned to the following groups: sham-operated, ischemia-reperfusion (I/R), ginsenoside Rb1+I/R, wortmannin(a specific PI3K inhibitor)+I/R, wortmannin drug vehicle (dimethyl sulfoxide, DMSO), wortmannin+sham, ginsenoside Rb1+ wortmannin +I/R. Infarct size was assessed by triphenyltetrazolium chloride staining. Plasma creatine kinase (CK), creatine kinase isoenzyme MB (CK-MB), lactate dehydrogenase (LDH), and troponin T levels were also measured. Akt phosphorylation expression was assessed by immunoblotting.


RESULTS
Ginsenoside Rb1 preconditioning reduced infarct size compared with that in the I/R group: 30 +/- 2.6% versus 51 +/- 2.7% (p < 0.01). Ginsenoside Rb1 preconditioning also markedly reduced the plasma CK, CK-MB, LDH and troponin T levels in blood. Akt phosphorylation expression increased after ginsenoside Rb1 preconditioning. These effects of ginsenoside Rb1 preconditioning were significantly inhibited by wortmannin.


CONCLUSIONS
This is the first study to demonstrate that ginsenoside Rb1 preconditioning has protective effects on myocardial ischemia and reperfusion injury, partly by mediating the activation of the PI3K pathway and phosphorylation of Akt.
Wang
Zhi
Z
Department of Anesthesiology, The Second Affiliated Hospital, Sun Yat-sen University, Guangzhou 510120, People's Republic of China.
Li
Min
M
Wu
Wei-kang
WK
Tan
Hong-mei
HM
Geng
Deng-feng
DF
D000730:Androstadienes / Q000494:pharmacology / Q000627:therapeutic use; D000818:Animals; D001794:Blood Pressure / Q000187:drug effects / Q000502:physiology; D015153:Blotting, Western / Q000379:methods; D003402:Creatine Kinase / Q000037:antagonists & inhibitors / Q000097:blood / Q000276:immunology; D052279:Creatine Kinase, MB Form / Q000037:antagonists & inhibitors / Q000097:blood / Q000276:immunology; D004121:Dimethyl Sulfoxide / Q000008:administration & dosage / Q000737:chemistry; D004334:Drug Administration Schedule; D004359:Drug Therapy, Combination; D036145:Ginsenosides / Q000037:antagonists & inhibitors / Q000737:chemistry / Q000627:therapeutic use*; D006339:Heart Rate / Q000187:drug effects / Q000502:physiology; D007275:Injections, Intravenous; D019157:Ischemic Preconditioning, Myocardial / Q000379:methods*; D007770:L-Lactate Dehydrogenase / Q000037:antagonists & inhibitors / Q000097:blood / Q000276:immunology; D008297:Male; D015394:Molecular Structure; D009203:Myocardial Infarction / Q000150:complications / Q000188:drug therapy*; D015428:Myocardial Reperfusion Injury / Q000150:complications / Q000188:drug therapy*; D005894:Panax / Q000737:chemistry; D014677:Pharmaceutical Vehicles / Q000737:chemistry; D019869:Phosphatidylinositol 3-Kinases / Q000378:metabolism / Q000494:pharmacology / Q000627:therapeutic use*; D010766:Phosphorylation / Q000187:drug effects; D010919:Placebos / Q000008:administration & dosage; D051381:Rats; D017207:Rats, Sprague-Dawley; D015398:Signal Transduction / Q000187:drug effects* / Q000502:physiology*; D013778:Tetrazolium Salts; D020107:Troponin T / Q000037:antagonists & inhibitors / Q000097:blood / Q000276:immunology; D000077191:Wortmannin
D000730:Androstadienes; D036145:Ginsenosides; D014677:Pharmaceutical Vehicles; D010919:Placebos; D013778:Tetrazolium Salts; D020107:Troponin T; C442759:ginsenoside Rb1; C009591:triphenyltetrazolium; D007770:L-Lactate Dehydrogenase; D019869:Phosphatidylinositol 3-Kinases; D003402:Creatine Kinase; D052279:Creatine Kinase, MB Form; D000077191:Wortmannin; D004121:Dimethyl Sulfoxide