title: Cyclovirobuxine D ameliorates acute myocardial ischemia by K(ATP) channel opening, nitric oxide release and anti-thrombosis.
abstract: 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.
authors.affiliation: Department of Molecular and Cellular Pharmacology, School of Pharmaceutical Sciences, Peking University, Beijing 100083, China.
authors.forename: Die
authors.initials: D
authors.lastname: Hu
authors.forename: Xiaoyan
authors.initials: X
authors.lastname: Liu
authors.forename: Yinye
authors.initials: Y
authors.lastname: Wang
authors.forename: Shizhong
authors.initials: S
authors.lastname: Chen
mesh_terms: D000208:Acute Disease; D000818:Animals; D000831:Animals, Newborn; D000068579:Celecoxib; D015687:Cell Hypoxia / Q000187:drug effects; D002470:Cell Survival / Q000187:drug effects; D002478:Cells, Cultured; D003328:Coronary Thrombosis / Q000517:prevention & control*; D052246:Cyclooxygenase 2 Inhibitors / Q000494:pharmacology; D004365:Drugs, Chinese Herbal / Q000494:pharmacology* / Q000627:therapeutic use; D042783:Endothelial Cells / Q000166:cytology / Q000187:drug effects / Q000378:metabolism; D004965:Estrogen Antagonists / Q000494:pharmacology; D005905:Glyburide / Q000494:pharmacology; D017202:Myocardial Ischemia / Q000378:metabolism / Q000503:physiopathology / Q000517:prevention & control*; D032383:Myocytes, Cardiac / Q000166:cytology / Q000187:drug effects / Q000378:metabolism; D019331:NG-Nitroarginine Methyl Ester / Q000494:pharmacology; D009569:Nitric Oxide / Q000378:metabolism*; D019001:Nitric Oxide Synthase / Q000037:antagonists & inhibitors / Q000378:metabolism; D026902:Potassium Channel Blockers / Q000494:pharmacology; D024661:Potassium Channels, Inwardly Rectifying / Q000819:agonists / Q000037:antagonists & inhibitors / Q000502:physiology*; D011720:Pyrazoles / Q000494:pharmacology; D051381:Rats; D017207:Rats, Sprague-Dawley; D013449:Sulfonamides / Q000494:pharmacology; D013629:Tamoxifen / Q000494:pharmacology
chemical_list: D052246:Cyclooxygenase 2 Inhibitors; D004365:Drugs, Chinese Herbal; D004965:Estrogen Antagonists; D026902:Potassium Channel Blockers; D024661:Potassium Channels, Inwardly Rectifying; D011720:Pyrazoles; D013449:Sulfonamides; D013629:Tamoxifen; D009569:Nitric Oxide; C032939:cyclovirobuxine D; D019001:Nitric Oxide Synthase; D000068579:Celecoxib; D005905:Glyburide; D019331:NG-Nitroarginine Methyl Ester