• Guang-Xing Bian, Gui-Gui Li, Yun Yang, Rui-Ting Liu, Jian-Ping Ren, Li-Qing Wen, Shao-Ming Guo, and Qiu-Jun Lu.
• Department of Pharmacology and Toxicology, Beijing Institute of Radiation Medicine, Beijing 100850, People's Republic of China.
• Biol. Pharm. Bull. 2008 Mar 1;31(3):458-63.

AbstractMadecassoside (MA), one of the principle terpenoids in Centella asiatica, has shown protect effect on isolated rat hearts and isolated cardiomyocytes against reperfusion injury in our previous studies. The aim of this study is to investigate if MA also protected against myocardial ischemia-reperfusion injury in vivo. The ischemia infarction model was established in rats. Left ventricular function was monitored during the ischemia-reperfusion period by a multi-channel recorder. After the ischemia-reperfusion process the infarcted areas were assessed. The levels of lactate dehydrogenase (LDH), creatinephosphokinase (CK), malondialdehyde (MDA), super-oxide dismutase (SOD) and C-reactive protein (CRP) in serum were determined. Cardiomyocytic apoptosis was measured by terminal-deoxynucleotidyl transferase mediated nick end labeling (TUNEL) staining. Pre-treatment with MA (50, 10 mg/kg) attenuated myocardial damage characteristic of decreasing infarct size, decreasing LDH and CK release. Activities of SOD were increased and MDA level increased obviously in control group whereas pretreatment with MA blunted the decrease of SOD activity, markedly reduced the level of MDA and the activity of CRP, and relieved myocardial cell apoptosis. These results suggest that MA has the protective effect on myocardial ischemia-reperfusion injury. This protection ability possibly due to its anti-lipid peroxidation, anti-inflammation and anti-apoptosis function and the enhancement of SOD activity.

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