| Atherosclerosis (AS) is a main disease that is harmful to our health, whichpathogeny and mechanism are still unknown. Ross pointed out that AS was a kindof pathology process which undergoing chronic inflammative course. Thedevelopment of AS are companied with inflammative reaction. In all the moleculemechanism of AS about inflammative course, we find both the structure and thefunction of EC have significant function. Thes studies consist of NO coming fromendothelium and CRP which is a inflammative factor. The courses are as follows:1.The change of CRP levels in the patients with hypercholesterolemiaThe levels of CRP in the patients with hypercholesterolemia were higher thanthe control group, and the levels of CRP were 9.80±1.30mg·L-1,9.63±4.37mg·L-1,13.54±3.68mg·L-1 and 3.54±1.25mg·L-1. The levels of CRP in the patientswith complexed hypercholesterolemia were13.54±3.68mg·L-1 and higher than inthe patients with simple hypercholesterolemia, and the levels of CRP were 9.80±1.30mg·L-1 and 9.63±4.37mg·L-1.There were no obvious differences of thelevels of CRP in three groups of differenced course of diseases and the levels ofCRP were 10.71±1.42mg·L-1,11.69±3.58mg·L-1 and 12.44±2.78mg·L-1.2. Building AS models of the rabbits and examining the expression ofNO and CRP in plasma in the normal diet and the cholesterol diet groups2.1 Building AS models2.1.1 Animals and groupsSixteen male rabbits were randomly divided into the normal diet and thecholesterol diet, each group was 8 and were fed for 16 weeks.2.1.2 Doing the pathology specimensAfter 16 weeks, all the rabbits were put to death and the aortas wereharvested for the pathologic morphology observations.2.1.3 Establishing hypercholesterolemiaThere were no obvious differences between TC and LDL in the normal dietand the cholesterol diet groups in plasma in 0 week (P>0.01) and there were noobvious differences between TC and LDL in the normal diet group in 8 and 16weeks compared with 0 week (P>0.01). There was obvious increase of TC andLDL in the cholestrol diet group after 8 and 16 weeks and there were obviousdifferences compared with 0 week (P<0.01).2.1.4 Naked view of ASThe naked observations were found that the structure of the arterial walls wasnormal and smooth, there was no formation of the atherosclerotic plaques in thenormal diet group. In the cholestrol diet group, generous flaw-whitestearo-matters projected over lumen and the arterial walls diffused intumescence.All those connected each other and formed atherosclerotic plaques .The ratio ofthe plaque area to the intima was 28.12±3.77%.2.1.5 Microscope view of ASIn the normal diet group, endothelial cells were integrated and lined up inorder, and intra-elasticity tunics were distinct and integrated, and the volume ofthe media smooth muscle cells and the arrangement were normal, and no foamcells and lipidoses were found in the intimas and the mediums, also the intimalthickness was 4.45±0.58 μm and the ratio of the intima to the medium was0.0537±0.007. In the cholesterol diet group, the endotheliocytes in the aorticintimas became swelling and degenerated, and the intimas were obviously thickwith the smooth muscle cell proliferation and the rearrangement, and lipidoses ofecto-cell and the macrophages can be find in the intimas and the mediums, and theintimal thickness was 67.47±7.13 μm which obviously became thick comparedwith the normal diet group and the ratio of the intima to the medium increasedcompared with the normal diet group and it was 0.878±0.370 (P<0.01).2.2 Measuring the expression of NO and CRP in the normal diet and thecholesterol diet groups in plasma2.2.1 Measuring the expression of NO in the normal diet and thecholesterol diet groupsThe levels of NO in the normal diet group and in the cholesterol diet group in0 weeks were 258.49±25.46μmol/L and 253.89±29.45μmol/L(P>0.01);Therewere no significant differences in the normal diet group and in the cholesterol dietgroup in 0 weeks;There were no significant differences in the normal diet groupin 0, 8 and 16 weeks(P>0.01) and the levels were 258.49±25.46μmol/L,261.52±20.64μmol/L and 253.88±31.48μmol/L;The levels of NO decreased in thecholesterol diet group in 8 weeks compared with 0 week, but there were nosignificant differences(P>0.05) and the levels were 220.48±36.13μmol/L and253.89±29.45μmol/L;The levels of NO obviously decreased in 16 weeks in thecholesterol diet group(P<0.01), and it was 179.46±9.17μmol/L.2.2.2 Measuring the expression of CRP in the normal diet and thecholesterol diet groupsThe levels of CRP in the normal diet group and in the cholesterol diet groupin 0 weeks were 3.71±0.74mg/L and 3.65±0.87mg/L(P>0.01);There were nosignificant differences in the normal diet group and in the cholesterol diet group in0 weeks;There were no significant differences in the normal diet group in 0, 8and 16 weeks (P>0.01) and the levels were 3.71±0.74mg/L, 3.68±0.69mg/L and3.92±0.84mg/L;The levels of CRP increased in the cholesterol diet group in 8weeks compared with 0 week(P<0.001) and the levels were 18.30±4.58mg/L and3.65±0.87mg/L;The levels of CRP obviously increased in 16 weeks comparedwith 8 weeks in the cholesterol diet group (P<0.001), and it was 31.73±8.70mg/L.3. Correlating NO and CRP expression with TC and LDL3.1 Correlating NO expression with TC and LDLThe dependent variable was TC and LDL separately, and the independentvariable was NO and linear regression analysis was used to distinguish thecorrelations of TC and LDL with NO. It was found that TC and LDL werenegatively correlated with NO and the coeffocient of product-moment correlationr was 0.428 and 0.484 (P<0.05).3.2 Correlating CRP expression with TC and LDLThe dependent variable was TC and LDL separately, and the independentvariable was CRP and linear regression analysis was used to distinguish thecorrelations of TC and LDL with CRP. It was found that TC and LDL werepositively correlated with CRP and the coeffocient of product-moment correlationr was 0.763 and 0.783(P<0.001).The dates were presented as mean ± SE, and statistical comparsions betweengroups were followed by the Student t test. The corresponding control value withP<0.05 considered statistically significant.The studies have shown:1. The serum CRP level in the patients with hypercholesterolemia is higherthan the control group, which indicates that TC and LDL may induce the releaseof inflammative factors and involve the information of AS.2. The espression of NO in serum have decreased in the rabbits of AS. Therewere a decreasing trend in 8 weeks compared with 0 week and there werestatistically significant in 16 weeks.3. The espression of CRP in serum have increased in the rabbits of AS. CRPlevels increased in the cholesterol diet group in 8 weeks compared with 0 week(P<0.001);The levels have obviously increased in 16 weeks compared with 8weeks in the cholesterol diet group.4. The expression of NO have the negtive correlation with TC and LDL, butthe expression of CRP have the positive correlation with TC and LDL.The significance of the studies:1. Through discussing the relationship of NO and CRP with AS, it has shownthat the happening of AS was companied with the injury of EC and the excessiverelease of inflammative factors. CRP, as the best representational inflammativefactor, has participated in the inflammative course.2. Through discussing the relationship of NO and CRP with TC and LDL, ithas shown that TC and LDL may influence both the release of NO and CRP inliver. The result has offered theoried evidence for preventing and treating ASthrough decreasing the levels of TC and LDL.3. The detecting of NO and CRP in serum have important meaning not onlyfor diagnosing the early AS but also for forecasting the happening, developing andending of it.
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