Effect of ginsenoside Rb3 on myocardial injury and heart function impairment induced by isoproterenol in rats.
The present study was designed to evaluate the effect of ginsenoside Rb3 on myocardial injury and heart function impairment induced by isoproterenol in rats. To induce myocardial ischemia, Sprague-Dawley rats were subcutaneously injected with isoproterenol (20mg/kg). Cardiac marker enzymes and antioxidative parameters in left ventricles were measured. Hemodynamic parameters were monitored and recorded as well. Histopathological examination of left ventricles was performed. It was found that the levels of creatine kinase and lactate dehydrogenase in isoproterenol-treated rats were significantly increased. The rats administrated with isoproterenol showed the declines in left ventricular systolic pressure, positive and negative maximal values of the first derivative of left ventricular pressure, and an elevation of left ventricular end diastolic pressure. Isoproterenol enhanced the content of malondialdehyde and decreased the activities of superoxide dismutase, catalase in left ventricles. Administration of ginsenoside Rb3 significantly ameliorated myocardial injury and heart function impairment induced by isoproterenol. The cardioprotective effect of ginsenoside Rb3 was further confirmed by histopathological examination. Ginsenoside Rb3 also alleviated the increase of malondialdehyde content and decrease of superoxide dismutase and catalase activities in left ventricles. The results indicated that ginsenoside Rb3 possesses the effect against isoproterenol-induced myocardial injury and heart function impairment, and that the mechanism of pharmacological action was related to the antioxidant activity of ginsenoside Rb3 at least in part.
Wang
Tian
T
Department of Pharmacology, School of Pharmacy, Jilin University, Changchun, 130021, China.
Yu
Xiaofeng
X
Qu
Shaochun
S
Xu
Huali
H
Han
Bing
B
Sui
Dayuan
D
D000818:Animals; D009202:Cardiomyopathies; D002374:Catalase / Q000378:metabolism; D003402:Creatine Kinase / Q000378:metabolism; D036145:Ginsenosides / Q000494:pharmacology*; D006321:Heart / Q000187:drug effects* / Q000503:physiopathology*; D006335:Heart Injuries / Q000139:chemically induced* / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology*; D006352:Heart Ventricles / Q000187:drug effects / Q000473:pathology; D007545:Isoproterenol / Q000494:pharmacology*; D007770:L-Lactate Dehydrogenase / Q000378:metabolism; D008297:Male; D008315:Malondialdehyde / Q000378:metabolism; D009206:Myocardium / Q000201:enzymology / Q000378:metabolism / Q000473:pathology; D051381:Rats; D017207:Rats, Sprague-Dawley; D013482:Superoxide Dismutase / Q000378:metabolism
D036145:Ginsenosides; D008315:Malondialdehyde; C044463:ginsenoside Rb3; D007770:L-Lactate Dehydrogenase; D002374:Catalase; D013482:Superoxide Dismutase; D003402:Creatine Kinase; D007545:Isoproterenol