Liu K, Abe T, Sekine S, Goto Y, Iijima K, Kondon K, Matsukawa M, Tian J, Wu W, Zhang B, Chen L, Zhang H, Zhang X, Zhao H, Song X
Department of Cardiovascular Surgery, Akita University School of Medicine, 1-1-1 Hondo, Akita 010-8543, Japan.
Ann Thorac Cardiovasc Surg. 1998 Aug;4(4):188-91.
Oxygen-derived free radicals play an important role in myocardial injury associated ischemia and reperfusion. To investigate whether ginsenosides, as an additive agent of cardioplegic solution, can decrease toxicity of oxygen free radicals in myocardial injury, a heterotopic heart transplantation model in Wistar rats was employed. St. Thomas II cold cardioplegia containing ginsenosides 80 mg/l was used in the experimental group. St. Thomas II cold cardioplegia alone was used in the control group. After global ischemia for 60 minutes and reperfusion for 30 minutes of a transplanted heart, SOD activity in the myocardium treated with ginsenosides was significantly higher than that in the control group (N=10, p< 0.01), whereas the MDA in the myocardium treated with ginsenosides were markedly lower than that of the control group (p< 0.01). The amounts of oxygen free radicals in the myocardium treated with ginsenosides were significantly lower than that of the control group (p <0.001). This study demonstrates that ginsenosides, as a proper additive agent of cardioplegic solution, can decrease toxicity of oxygen free radicals, suggesting one of the mechanisms for its protective effects against myocardial ischemia and reperfusion injury.