Abstract
BackgroundThe impact of L-arginine on atherogenesis and its ability to prevent endothelial dysfunction have been studied extensively during the past years. L-arginine is a substance for nitric oxide synthesis which involves in apoptosis. Hypercholesterolemia promotes endothelial dysfunction, and it is hypothesized that L-arginine prevents endothelial dysfunction through endothelial cells apoptosis inhibition. To test this hypothesis, thirty rabbits were assigned into two groups. The control group received 1% cholesterol diet for 4 weeks, and the L-arginine group received same diets plus 3% L-arginine in drinking water.ResultsNo significant differences were observed in cholesterol level between two groups, but the nitrite concentration in L-arginine group was significantly higher than other group (control group: 11.8 ± 1; L-arginine group: 14.7 ± 0.5 μmol/l); (p < 0.05). The aorta score of fatty streak in control group was 0.875 ± 0.35, but no fatty streak lesion was detected in L-arginine group (p < 0.05). The number of intimal apoptotic cells/500 cells of aorta in two groups of experiment were statistically different (control group: 39.3 ± 7.6; L-arginine group: 21.5 ± 5.3) (p < 0.05).ConclusionThe inhibition of endothelial cells apoptosis by L-arginine restores endothelial function in a model of hypercholesterolemia.
Highlights
The impact of L-arginine on atherogenesis and its ability to prevent endothelial dysfunction have been studied extensively during the past years
The statistical analyses indicate that no significant difference was observed between the cholesterol levels of two groups, but the nitrite concentration in L-arginine group was significantly higher than control group (p < 0.05)
Fatty streak formation The score of aorta fatty streak in first group was 0.875 ± 0.35, but no fatty streak lesion was detected in L-arginine group
Summary
The impact of L-arginine on atherogenesis and its ability to prevent endothelial dysfunction have been studied extensively during the past years. Hypercholesterolemia promotes endothelial dysfunction, and it is hypothesized that L-arginine prevents endothelial dysfunction through endothelial cells apoptosis inhibition. To test this hypothesis, thirty rabbits were assigned into two groups. Lipids in Health and Disease 2008, 7:27 http://www.lipidworld.com/content/7/1/27 to promote endothelial dysfunction (ED) and atherogenesis can induce vascular cell apoptosis [10]. A study in monkeys revealed that vascular ED was present without evidence of atherosclerosis, which may be due to endothelial apoptosis [11]. Intervention with NO donor; L-arginine, has induced beneficial effects on atherosclerosis [15] These findings strongly support the current clinical concept that ED precedes plaque formation and disease progression in patients [16]
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