Effect of ginsenoside Rh1 on myocardial injury and heart function in isoproterenol-induced cardiotoxicity in rats.
The present study was designed to investigate the effect of ginsenoside Rh1 on myocardial injury and heart function in isoproterenol-induced cardiotoxicity in rats. Sprague-Dawley rats were subcutaneously injected with isoproterenol (20 mg/kg). Cardiac marker enzymes in serum, antioxidative parameters and inflammatory cytokines in left ventricles were measured. Hemodynamic parameters were monitored and recorded as well. Histopathological examination of left ventricles was performed. It was found that creatine kinase-MB (CK-MB) activity and troponin T level in isoproterenol-treated rats were significantly increased. Isoproterenol caused declines of 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 (MDA), tumor necrosis-α (TNF-α), interleukin-1β (IL-1β) and decreased the activities of superoxide dismutase (SOD), catalase, and glutathione peroxidase (GSH-Px) in left ventricles. Ginsenoside Rh1 significantly ameliorated myocardial injury and heart function impairment induced by isoproterenol. The cardioprotective effect of ginsenoside Rh1 was further confirmed by histopathological examination. Ginsenoside Rh1 also partially inhibited the increase of MDA, TNF-α, IL-1β contents and the decrease of SOD, catalase, and GSH-Px activities in left ventricles. The results indicated that ginsenoside Rh1 possessed the effect against isoproterenol-induced cardiotoxicity, and that the mechanism of pharmacological action was related to regulating the activities of SOD, catalase, and GSH-Px and decreasing the contents of TNF-α and IL-1β.
Department of Cardiovascular Medicine, Yantaishan Hospital, Yantai, China.
Yusheng
Y
Gai
Zhigang
Z
Ma
Xiaofeng
X
Yu
Shaochun
S
Qu
Dayuan
D
Sui
D000818:Animals; D001794:Blood Pressure / Q000187:drug effects; D002316:Cardiotonic Agents / Q000494:pharmacology* / Q000633:toxicity*; D003402:Creatine Kinase / Q000097:blood; D004195:Disease Models, Animal; D036145:Ginsenosides / Q000494:pharmacology*; D006321:Heart / Q000187:drug effects* / Q000503:physiopathology; D006352:Heart Ventricles / Q000187:drug effects / Q000378:metabolism / Q000473:pathology; D007545:Isoproterenol / Q000633:toxicity*; D008297:Male; D017202:Myocardial Ischemia / Q000139:chemically induced / Q000503:physiopathology / Q000517:prevention & control*; D009206:Myocardium / Q000378:metabolism / Q000473:pathology; D018384:Oxidative Stress / Q000187:drug effects; D010088:Oxidoreductases / Q000378:metabolism; D005894:Panax; D051381:Rats; D017207:Rats, Sprague-Dawley; D020107:Troponin T / Q000097:blood; D018487:Ventricular Dysfunction, Left / Q000139:chemically induced / Q000188:drug therapy
D002316:Cardiotonic Agents; D036145:Ginsenosides; D020107:Troponin T; C425564:ginsenoside Rh1; D010088:Oxidoreductases; D003402:Creatine Kinase; D007545:Isoproterenol