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Cyclovirobuxine D Ameliorates Acute Myocardial Ischemia by K(ATP) Channel Opening, Nitric Oxide Release and Anti-Thrombosis

Cyclovirobuxine D Ameliorates Acute Myocardial Ischemia by K(ATP) Channel Opening, Nitric Oxide Release and Anti-Thrombosis

Die Hu, Xiaoyan Liu, Yinye Wang, Shizhong Chen

Eur J Pharmacol. 2007 Aug 13;569(1-2):103-9.

PMID: 17555743

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.

Chemicals Related in the Paper:

Catalog Number	Product Name	Structure	CAS Number	Price
CS31041034	Celecoxib Related Compound D			Price

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