cyclovirobuxine-d and Myocardial-Ischemia

Cyclovirobuxine D is an active compound extracted from Buxus microphylla, which has been used for treating acute myocardial ischemia in China. The present study was to investigate its mechanism on myocardial ischemia. Cyclovirobuxine D significantly increased cardiomyocytes viability injured by oxidation or hypoxia. It significantly reduced the infarct size induced by ligating the coronary artery in rats, and the effect was almost abolished by glibenclamide, a blocker of ATP sensitive potassium channel, but it was not influenced by cyclooxygenase-2 inhibitor celecoxib or estrogen receptor antagonist tamoxifen. In addition, cyclovirobuxine D significantly protected rat aorta endothelial cells against hypoxia and enhanced nitric oxide (NO) release from endothelial cells, which was inhibited by nitric oxide synthase (NOS) inhibitor N-nitro-L-arginine methyl ester (L-NAME). Furthermore, cyclovirobuxine D significantly decreased the weight of venous thrombus in rats. In conclusion, the action mechanism of cyclovirobuxine D on myocardial ischemia may be related with its cytoprotection, K(ATP) channel opening, NO generation stimulating and venous thrombosis inhibiting.

Topics: Acute Disease; Animals; Animals, Newborn; Celecoxib; Cell Hypoxia; Cell Survival; Cells, Cultured; Coronary Thrombosis; Cyclooxygenase 2 Inhibitors; Drugs, Chinese Herbal; Endothelial Cells; Estrogen Antagonists; Glyburide; Myocardial Ischemia; Myocytes, Cardiac; NG-Nitroarginine Methyl Ester; Nitric Oxide; Nitric Oxide Synthase; Potassium Channel Blockers; Potassium Channels, Inwardly Rectifying; Pyrazoles; Rats; Rats, Sprague-Dawley; Sulfonamides; Tamoxifen

To study the cardiac protection of Cyclovirobuxinum D (Cvb-D) in rats model.. The rats were subjected to left main coronary artery occlusion. The change about S-T segment, the area of myocardial injury (necrotic and ischemic areas), the amount of cardiac tissue malondialdehyde (MDA), the cardiactissue creatine phosphokinase (CPK) and the cardiac tissue superoxide dismutase (SOD) activation were measured.. Compared to the model group, Cvb-D (1.1 mg/kg, 2.2 mg/kg dos-age) significantly reduce myocardial damage, reduce myocardial ischemia mode rats' sigma s-t of ECG, significantly reduce cardiac tissue CPK activation and MDA content, raise the cardiac tissue SOD activation in the rats with myocardial ischemia.. Cvb-D is effective in treatment of myocardial ischemia in rats.

Topics: Animals; Buxus; Cardiotonic Agents; Coronary Vessels; Dose-Response Relationship, Drug; Drugs, Chinese Herbal; Electrocardiography; Female; Ligation; Male; Malondialdehyde; Myocardial Ischemia; Myocardium; Plants, Medicinal; Rats; Rats, Sprague-Dawley; Superoxide Dismutase

To explore the pharmacology actions of Cyclovirobuxinum D (Cvb-D) for the myocardial ischemia and study its possible mechanism.. The rats were given orally with Cvb-D 0.55 g/kg, 1.1 g/kg and 2.2 g/kg per day, for 21 days. The myocardial ischemia model were induced by isoprenaline. The rats ECG, serum CPK, LDH, FFA and myocardium tissue SOD, MDA level were detected.. Cvb-D could significantly reduce myocardial ischemia model induced by isoprenaline rats' sigmaJ of ECG, shorten ECG resume time, reduce serum FFA content, serum CPK, LDH activation, reduce cardiac tissue MDA content, raise the cardiac tissue SOD activation.. Cvb-D can decrease the release of FFA, CPK, LDH and improve the model rats' myocardium MDA, SOD level. It may be some of mechanisms of its anti-myocardial ischemia effect.

Topics: Animals; Buxaceae; Drugs, Chinese Herbal; Isoproterenol; Male; Myocardial Ischemia; Myocardium; Plants, Medicinal; Rats; Rats, Sprague-Dawley