TY - JOUR
T1 - Ginsenoside Rb1 preconditioning protects against myocardial infarction after regional ischemia and reperfusion by activation of phosphatidylinositol-3- kinase signal transduction
AU - Wang, Zhi
AU - Li, Min
AU - Wu, Wei Kang
AU - Tan, Hong Mei
AU - Geng, Deng Feng
N1 - Funding Information:
Project supported by the National Basic Research Program of China (a.k.a. 973 Program) (No.2005CB523305).
Funding Information:
Acknowledgments The present work was supported by research grants (the National Basic Research Program of China, 2005CB523305) to Dr. Wei-kang Wu from the National Science Council, China. We thank Dr. Wen Wang and Dr. Martha Dahlen for critical review of this manuscript.
PY - 2008/12
Y1 - 2008/12
N2 - 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 preconditoning were significantly inhibited by wortmannin. Conclusion: 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.
AB - 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 preconditoning were significantly inhibited by wortmannin. Conclusion: 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.
KW - Akt
KW - Ginseng
KW - Ginsenoside Rb1
KW - Infarct size
KW - Myocardial reperfusion injury
KW - Phosphatidylinositol-3-kinase
KW - Wortmannin
UR - http://www.scopus.com/inward/record.url?scp=55949136010&partnerID=8YFLogxK
U2 - 10.1007/s10557-008-6129-4
DO - 10.1007/s10557-008-6129-4
M3 - Journal article
C2 - 18679782
AN - SCOPUS:55949136010
SN - 0920-3206
VL - 22
SP - 443
EP - 452
JO - Cardiovascular Drugs and Therapy
JF - Cardiovascular Drugs and Therapy
IS - 6
ER -