| Objective:To establish the model of rabbit with hypercholesterolaemia-atherosclerosis and observe the changes of blood lipid density, and the positive expression of platelet/endothelial cell adhesion molecule-1 (platelet-endothelial cell adhesion molecule, PECAM-1) and P-selectin (P-selectin, CD62P) in the rabbit ascending aorta tissues. Then we will investigate the influence of atorvastain to them.Methods:30 healthy male New-Zealand white rabbits, body weight (2.0±0.2) kg, 4-months-age, were randomly divided into three groups:normal control group (group A), high-cholesterol diet group (group B) and high-cholesterol diet plus atorvastatin treatment group (group C).Each group had 10 rabbits,sub-cage feeding for 16ws. After feeding for 16ws,the empty stomach blood samples of all the rabbits were collected through ear vein at awake state(fasting about 12-hour), were centrifugalizated (3000rpm,10min).The blood serum was stored at-20℃. Density of the total cholesterol (TC), low-density lipoprotein cholesterol (LDL-C), and so on were evaluated by Hitachi 7600 automatic biochemical analyzer. The inferior segments of ascending aorta tissues were observated by pathomorphology. All superior segments of scending aorta tissues were to determine the expression of PECAM-1 and P-selectin by RT-PCR, and the results were to do semi-quantitative analysis by UVP gel imaging system package Vision Works LS software.-d high-cholesterol diet to establish atherosclerosis model. The total number of experimental animals were 30.To the end of the trial,2 rabbits of Group B died for diarrhea,1 for respiratory tract infections and 1 for some reasons; 2 rabbits of Group C died for diarrhea and 1 for parasitic infection; and 2 rabbits of Group A died for some reasons. The animal livability was 70.0%. At the end of the trial, both eating and nutrition were in good condition in surviving rabbits of each group, and no heart failure symptoms. But the mortality was higher just by high-cholesterol diet to establish atherosclerosis model.2) The detection of blood lipids level:The levels of TC, TG, LDL-C, VLDL-C were greater (P<0.05) in Group B than those in Group A and Group C; the level of HDL was lower (P<0.05) in Group B than those in Group A, but higher than those in Group C (P< 0.05); And the levels of TC, TG, LDL-C, VLDL-C were also greater (P <0.05) in Group C than those in Group A.3) The ascending aorta tissues used for HE staining and observed under light microscope:The HE staining in Group A showed no obvious abnormalities,the wall structure was clear, the intimae surface was smooth, the endothelial cells were continuous integrity and was non-lipid deposition under the endothelium. The HE staining in Group B showed thicker intimae, endothelial cell loss or discontinuity, under endothelium which were infiltrated with many foam cells and inflammatory cell. Plaque could be seen within lipid deposition and smooth muscle cells proliferation. The HE staining in Group C, there had foam cells and inflammatory cells under endothelium, the cell structure and morphology was relative rules, but the degree and extent of lesions were much lesser than Group B.4) The positive expression of PEC AM-1 at ascending aorta:The expression of PEC AM-1 was significantly higher in Group B than in Group A; the expression of PEC AM-1 was lower in Group C than in Group B, but still higher than in Group A. 5) The positive expression of P-selectin at ascending aorta:The expression of P-selectin was also significantly higher in Group B than in Group A; the expression of P-selectin was lower in Group C than in Group B, but still higher than in Group A.Conclusions:1, Our study used high-cholesterol diet as feeding methods, and we successfully established atherosclerotic models. This way has a high success rate, but model time was too long.2, Atorvastatin can effectively regulate lipid metabolism.3, PEC AM-1 and P-selectin might be the two important atherogenic adhesion molecules. The adhesion molecules could promote the migration of inflammatory cells, further exacerbated the inflammatory response and participated the pathogenesis of atherosclerosis.4, Atorvastatin can reduce the expression of this two adhesion molecules, PECAM-1 and P-selectin.
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