Effects Of Clopidogrel On Expressions Of Vascular Wall NF-κB And Serum Hypersensitivity C-Responsive Protein In Atherosclerotic Rabbits

Objective: To observe the effects of ADP receptor blocker clopidogrel on the level of serum hypersensitivity C-responsive protein(hs-CRP),the expressions of vascular wall nuclear factor-kappaBp65mRNA(NF-κBp65mRNA) and p65 subunit,and the plaque area of aorta and the neointima thickness in atherosclerotic rabbits.Methods: Thirty-six New Zealand male rabbits were randomly divided into normal control group(NC group, n=9), high-cholesterol group(HC group,n=9), high-cholesterol plus fluvastatin group(CF group,n=9) , high-cholesterol plus clopidogrel group(CC group,n=9) and then were fed for 12 weeks.At the beginning of the experiment,the levels of serum TC,TG, LDL, HDL and hs-CRP were examined respectively by standard enzymatic assay and enzyme-linked immunosorbent assay and again at end of the experiment. Enzyme-linked immunosorbent assay, situ hybridization and histomorphometry analysis were employed respectively to detected the level of p65 subunit, the expression of NF-κBp65mRNA in vascular wall atherosclerotic plaque and the plaque area of aorta and the neointima thickness.Result: There was no significant difference in the levels of serum lipids and hs-CRP among the four proups at the beginning of the experiment.At the end, the levels of the serum TC,LDL,HDL, serum hs-CRP and the expressions of vascular wall NF-κBp65 mRNA and p65 subunit, the neointima thickness and plaque area of aorta in the HC,CC and CF groups were significantly increased compared with the NC group(P<0.05);There was no significant difference in serum lipids between the CC group and the HC group, but the level of serum hs-CRP and the expressions of vascular wall NF-κBp65 mRNA and p65 subunit, the neointima thickness and plaque area of aorta in the CC group were significantly decreased compared with the HC group(P<0.05).Conclusion: Clopidogel could decreased inflammatory reaction in atherosclerotic plaque and hinder the development of atherosclerosis in a certain extent by hindering platelet activation and reducing the expression of NF-κB and the production of hs-CRP.