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The present study investigated the effect of lovastatin, a HMG-CoA reductase inhibitor, on the regression or progression of atherosclerosis and on the susceptibility of LDL to oxidation in vitro in cholesterol-fed rabbits. New Zealand White Rabbits were fed 1 % cholesterol for 4 weeks, and 0.5% cholesterol for additional 12 weeks. One subgroup of cholesterol-fed rabbits was treated with lovastatin (10 mg/day) from week 5-16. By the method of Cu2+-mediated LDL oxidation, oxidative susceptibility of LDL was measured at 4 and 16 weeks of the experimental period. Cholesterol-feeding induced a marked increase in oxidative susceptibility of LDL. Treatment with lovastatin had no effect on lag time, maximal diene production, or diene production rate, even though it reduced plasma total cholesterol concentrations by about 50%. At the time of sacrifice, the extent of atherosclerotic lesions was measured by morphometric analysis of intimal plaque area in the common carotid ru1eries. Carotid intimal plaque ru·ea was 15.8±4.6% after 4 weeks of cholesterol-feeding and 44.0±5.2% after 16 weeks. Lovastatin suppressed the progression of plaque formation (to 27 .0±5.1 %) but did not induce regression. These data suggest that lovastatin can slow the progression of atherosclerotic plaque formation in rabbits induced by cholesterol-feeding without decreasing the oxidative susceptibility of LDL.
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