| Objective: The aim of this study was to clarify the molecular mechanisms ofpolicosanol against atherosclerosis through studying the pre-intervention effect ofpolicosanol against arterial atherosclerosis in rats. We measured and investigatedseveral indicators in the rats, including the lipid levels, the changes of seruminflammation markers including high sensitivity C-reactive protein(hs-CRP), thedescending aortic electron microscopy, and the phosphorylation expression levels ofP38MAPK(an atherosclerotic plaque).Methods:40SD rats were divided into four groups at average: normal group,atherosclerosis group(AS group), atorvastatin group and policosanol group. Theatherosclerosis rat model was prepared using intraperitoneal injection of Vit D3withhigh cholesterol diet for12weeks.(a) Measured the effect of on rat descending aorticatherosclerotic plaque through transmission electron microscope;(b) Investigatedthe changes of serum inflammation markers including high sensitivity C-reactiveprotein(hs-CRP) through ELIISA;(c) Investigated the effect on serum and lipid levelsin CHO-PAP Method;(d) Investigated the P38MAPK phosphorylation expressionlevels on the effect of policosanol through Western Blot Method.Results:(a) The AS rats lost endothelial cells, the collagen fibers was significantlyincreased, disorderly arranging with partly fibrinolysis, sedimentary lipidgranuleunder endothelium, SMCs arranged in disorder, mitochondrial swelling, indicatingearly atherosclerosis. The normal rats’ SMCs arranged in orderly and the endotheliumremained intact. The policosanol rats and the atorvastatin rats with less endothelialcells, but the former had more collagenous fibers and lipin deposition.(b) The serum Hs-CRP in AS, policosanol and atorvastatin rats was higher than thenormal rats (P <0.05). The Policosanol rats received less effect on inflammationreducing than the atorvastatin rats (P <0.05).(c) The TC and LDL-C levels in AS, policosanol and atorvastatin rats was higher than the normal rats (P <0.05), indicating the success of this experimental model. ThePolicosanol rats received higher HDL-C increase than the atorvastatin rats (P <0.05),but no significant differences on reducing TC and LDL-C.(d) The expression of P38MAPK phosphorylated proteins had the highest and lowestrecords separately in the AS rats and the normal rats. The protein expressiondifferences between policosanol rats and the rest had statistically significant (P<0.05).Conclusion:(a) The normal rats had intact endothelial cells, the AS rats showedchanges of early atherosclerosis, the policosanol rats and atorvastatin rats had mildatherosclerosis. The policosanol rats showed suppression on AS progress to certainextent.(b) The serum Hs-CRP levels in policosanol was lower than the AS rats, indicatingthat policosanol made anti-inflammatory effect by reducing the Hs-CRP.(c) The policosanol rats had lower serum TC and LDL-C than the AS rats. Comparingto the atorvastatin rats, the policosanol rats showed stronger in serum HDL-Cincreasing and no difference in decreasing serum TC and LDL-C. The facts aboveindicate that the policosanol had the lipid-lowering efficacies.(d) The expression of P38MAPK phosphorylated proteins was lower in policosanolrats and atorvastatin rats than that in AS rats, indicating that policosanol can reducethe expression of P38MAPK phosphorylated proteins, and the P38MAPKphosphorylated signal pathway may play a role in policosanol’s anti-inflammatorymechanism. |
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