To Explore The Inhibition Of Polyinosinic Acid Combined Statin On Cholesterol Crystals As Well As Expression Of Hs-CRP In Atherosclerotic Rabbits

Objective To explore the inhibition of Polyinosinic acid combined statin on Cholesterol crystals as well as expression of hs-CRP in atheroscler.Methods Mass of2.0±0.2kg thirty male New Zealand white rabbits were randomly divided into five groups after seven days by the regular feed processing: control group, hypercholesterol group, poly I group, fluvastatin group, association (poly I and fluvastatin) group (n=6).Except control group, the others were strained by balloon on abdominal aortic after they received general anesthesia by3%pentobarbital sodium at the beginning.After12weeks, rabbits were sacrificed and abdominal aortas were removed to examined pathological changes and Elisa method were determined in the expression of hsCRP plaques organizationResults Pathological changes of abdominal aortic:(1) control group:ascular intima endothelial cells showed no lack and connectioned with the internal elastic plate close, the endothelial cell layer continuity; vascular smooth muscle cells arranged in neat cytoplasm eosinophilic, HE staining is red, no significant lipid deposition, also no cholesterol crystals formed (Fig.1A).(2) hypercholesterol group, vascular intima endothelial cells fell off and there was visible atheromatous plaque formation. Under the fibrous cap, large numbers of amorphous necrotic disintegrating products could be saw with large amounts of Cholesterol crystals, foam cells and lymphocytes; Due to atheroma oppression, smooth muscle cells shrink and central film thinning. Eosinophilic cytoplasm disordered arrangement of smooth muscle cells, alternative to a large number of foam cells. Cytoplasmic staining of foam cells, filled with lipid vacuoles. Part of the atheromatous plaque at the bottom and the edge of the granulation tissue neovascularization, accompanied by lymphocyte infiltration of inflammatory cells (Figure1B).(3) fluvastatin group, endothelial cells part fell off. Beneath the vascular intima, there were scattered and irregular plaques with a small amount of foam cells and a little inflammatory cells and Cholesterol crystals which less than polyI group.(4) poly I group, endothelial cells part fell off and there had a lot of foam cells below fibrous cap,as well as inflammatory cells, and had Cholesterol crystals which less than hypercholesterol group.(5) association group, there had a obvious weaker atherosclerosis than hypercholesterol group. Its ascular intima slightly thickened, and had a little foam cells, smooth muscle ranked tidily, and had no obvious Cholesterol crystals. Elisa results:Compared with the control group, the expression of the hypercholesterol group hsCRP was significantly increased (p<0.01). Compared with the hypercholesterol group, the expression levels of statins and combination groups decreased significantly (p<0.01), the amount of poly I group hsCRP expression also decreased (p<0.01). Compared with Poly I group, the association group to reduce the role of hsCRP expression more significantly (p<0.01). Not distinctive expression levels between the statin group and the association group (p>0.1).Conclusion (1) Poly I combined fluvastatin can significantly inhibit the development of atherosclerosis, maximum reduce the amount of cholesterol crystal formation, which stronger than fluvastatin or Poly I.(2) Poly I combined fluvastatin inhibit the expression of the role of hsCRP in atherosclerotic plaque tissue most obvious, which stronger than fluvastatin or Poly I.(3) Poly I combined with statin anti-artery atherosclerosis role still needs more large-scale experiment to study...