Biol. Pharm. Bull. 28(7) 1239—1243 (2005)

lial nitric oxide (NO) inhibits platelet aggregation, thrombogenesis, leukocyte adhesion, and proliferation of vascular smooth muscle cells. Endothelial dysfunction that is closely related with impaired NO actions may represent a early stage of vasculopathy leading to atherosclerotic cardiovascular disorders. Accordingly, chronic inhibition of NO synthesis by administration of high dosage of N-nitro-Larginine methyl ester (L-NAME) to rats induces an early hypertensive state associated with vascular inflammation in a week, and then severe atherosclerosis in coronary artery in 4—8 weeks. Impaired release of NO from vascular beds results in increased leukocyte–endothelium interaction via up-regulation of endothelial cell adhesion molecules which include E-selectin, intercellular adhesion molecule-1 (ICAM-1), and vascular cell adhesion molecule-1 (VCAM-1). Under these conditions, numerous leukocytes adhere to vascular endothelium and transmigrate the endothelium, thus aggravating endothelial dysfunction and tissue injury. On the contrary, systemic administration of NO donors to NO-deficient animals preserves endothelial function and attenuates pathological interactions between circulating leukocytes and vascular endothelium. Sorbus commixta cortex (MSC) (Malaceae) has long been used in the field of traditional Oriental medicine as a tonic and for the control of cough, asthma, and other bronchial disorders. Recently, MSC was shown to have a potent radical scavenging activity. We also made an observation that MSC relax vascular smooth muscle via up-regulation of endothelium-dependent NO-cyclic guanosine-3 ,5 -cyclic monophosphate (GMP) pathway. This pharmacological effect of MSC on vascular tissue may be useful for the treatment of various cardiovascular diseases such as hypertension and atherosclerosis. Therefore, we aimed to investigate in vivo anti-inflammatory and anti-atherosclerotic activities of MSC in a rat model of NO-deficient atherosclerosis.