Objective: We aimed to explore the effects of lipid smoothness on the progression and vulnerability of atherosclerotic plaques.
Approach: 24 rabbits were divided into three groups randomly. Group 1 was given standard chow diet; group 2 was fed with cholesterol-rich diet; for group 3, subjects were planned to take cholesterol-rich diet at the first phase for 12 weeks and during the second phase, low-fat and cholesterol-rich diet was then applied alternately every three weeks till the end of the experiment. Lipid profiles, inflammatory factors, endothelium functions, pathological and histological changes were examined. Expressions of matrix metalloproteinase-9 and lectin-like oxidized LDL receptor-1 were measured by immunohistochemical staining.
Results: According to data collected during the whole experiment, lipid smoothness index of group 3 was the lowest. Compared with group 2, statistics of the group 3 indicated that: the development of plaques progressed faster; the plaque area and plaque thickness (53.53[22.6]% vs 33.90[24.91]% , 800.38[98.25]µm vs 675.00[109.67]µm) were higher while the fibrous cap thickness (103.50[45.66]µm vs 295.83[97.90]µm) was lower; hs-CRP (0.53[0.07]mg/dL vs 0.45[0.06]mg/dL), interleukin-18 (186.01[8.41]ng/L vs 158.08[2.37]ng/L), OX-LDL (177.15[5.93]µg/L vs 139.57[2.35] µg/L) and endothelin-1 (164.66[9.54]ng/L vs 131.52[4.39]ng/L) were higher while nitric-oxide (22.41[1.69]µmol/L vs 27.23[1.36]µmol/L) was lower; expressions of matrix metalloproteinase-9 (IOD: 37375.87[5634.52] vs 20956.57[4616.93]) and lectin-like oxidized LDL receptor-1 (IOD: 45213.04[16653.81] vs 21921.68[6142.32]) were higher.
Conclusions: Lipids fluctuation could accelerate the progression and vulnerability of atherosclerotic plaques through worsening arterial endothelium dysfunction and inflammatory reactions.