ABSTRACT
Materials and Methods Animal Preparation and Experimental Procedures. Male New Zealand white rabbits, 3 mo old and weighing 2.5-3.0 kg, were housed in the animal center of the Taipei Veterans General Hospital, Taiwan. After 1 wk of consuming a commercial rabbit chow diet (Scientific Diet Services, Essex, UK), the rabbits were fed a 2% high cholesterol diet (Purina Mills, St. Louis, MO). In different experiments (36-38), the rabbits underwent various treatments, including the following: (i) no drug treatment as the control group (group C), (ii) probucol treatment with oral ingestion of probucol [0.6 g/(kg body
magnolol treatment with daily intramuscular injection of magnolol (1 µg/kg body, group M) (36), (iv) SM treatment with oral ingestion of SM extract [4.8 g/(kg body
SM] (37), and (v) EGb treatment with oral ingestion of EGb tablet [16 mg/(kg body
and EGb groups were the experimental groups. The investigation conformed with NIH guidelines. The protocol was approved by the Animal Care and Use Committee of National Yang-Ming University, Taipei, Taiwan. The magnolol, SM, and EGb doses were calculated according to the literature (27,31). Rabbits had free access to water. Three weeks after starting the experiment, the rabbits were anesthetized
Introduction Percutaneous transluminal coronary angioplasty (PTCA) is a widely used, well-accepted treatment for coronary stenotic lesions resulting from atherosclerosis. Restenosis occurs in 30-50% of patients within the first 6 mo of PTCA (1). The formation of intimal hyperplasia after balloon angioplasty is due mainly to the phenotypic conversion and proliferation of smooth muscle cells as well as the accumulation of activated macrophages and foam cells (2,3). The development of atherosclerotic and restenotic lesions is also considered to be an immune-inflammatory reaction, triggered by a cascade of activation of growth factors and cytokines (4,5). Among them, the important mediators of monocyte recruitment into the vascular wall include monocyte chemotactic protein-1 (MCP-1) and interleukin 1β (IL1β). MCP-1, which is secreted by vascular and circulating cells, induces undifferentiated monocyte migration to sites of active inflammation or injury (6,7). IL-1β is a proinflammatory cytokine, which participates actively in stimulating vascular smooth muscle cell proliferation (8), leukocyte adhesion to the endothelium (9), modulation of low density lipoprotein (LDL) metabolism (10), and secretion of extracellular matrix proteins (11). These findings suggest that MCP-1 and IL-1β might play important roles in the pathogenesis of vascular lesion formation.
