| Objective Atherosclerosis(atherosclerosis, AS) is the pathological basis of coronary heart disease, abnormal blood lipid metabolism, oxidative stress injury and inflammation play an important role in the occurrence and development of the AS, so the above link for effective prevention and control of intervention is AS an important method. Coenzyme Q10 is a common antioxidant, scavenging free radicals and prevent lipid peroxidation effect, but its impact on the AS and mechanism remains unclear. Points two parts of clinical and basic research, this study first discusses coronary heart disease patients serum paranoxonase 1(paranoxonase,PON1) and lipoprotein- associated phospholipase A2(lipoprotein- associated phospholipase A2, LP- PLA2) activity and the correlation of coronary lesion counts and atheromatous plaque stability. Then by building in the rat model of atherosclerosis, coenzyme Q10 was given from the perspective of the pathological morphology to observe the effects of coenzyme Q10 in artery atheromatous plaque, then further research on coenzyme Q10 on the AS model rats blood lipid level, oxidative stress and inflammatory factor, the influence of the correlation of coenzyme Q10 treatment AS disease to provide some theoretical and experimental basis.Methods According to the coronary angiography results divided the patients into coronary heart disease group(n=88) and control(n=32). Patients with coronary heart disease(CHD) according to coronary artery lesion counts are divided into: 1) single lesion; 2) double branch lesions; 3) three lesions. Stable angina means plaque stability, myocardial infarction means plaque instability. Serum PON1 and LP-PLA2 activity among groups were compared,relationship between PON1?LP-PLA2 activity and coronary lesions degree and plaque stability was analysed. Seven Wistar rats were treated as control group(group B). Then 31 rats were intraperitoneal injected with vitamin D3 + intraperitoneal injected Ovalbumin + fed with high-fat diet to make atherosclerosis model rats. It was proved to be successful with HE results of random three of the 31 rats. Then the residual AS model rats were randomly divided into 4 groups(seven of each group): 1) the AS model control group(group A); 2) coenzyme Q10 treatment group(group C); 3) atorvastatin treatment group(group D); 5)coenzyme Q10 + atorvastatin treatment group(group E). control group was given conventional breeding.Other groups were given high-fat diet. Then given drug 8 weeks, group A and group B were given physiological saline every day, group C was given coenzyme Q10 30 mg/kg/d, group D was given atorvastatin 5 mg/kg/d, group E was given coenzyme Q10 30 mg/kg/d + atorvastatin 5 mg/kg/d. The rats were sacrificed after 8 weeks administration.5 ml blood was drawn from abdominal aorta of rats and serum was separated.The serum total cholesterol(TC),triglycerides(TG) and low-density lipoprotein cholesterol(LDL), high-density lipoprotein cholesterol(HDL), apolipoprotein B(APOB) were detected by enzymatic assays with use of an automated biochemical analyzer.Blood lipid ratio(TCH/HDL, LDL/HDL) were calculated. Serum oxidized HDL(ox-HDL) and malondialdehyde(MDA) was detected by enzyme-linked immunosorbent assay(ELISA). Serum PON1 activity and LP-PLA2 activity was detected with use PON1 and LP-PLA2 kits. Take the aortic arch stained with hematoxylin to observe the atherosclerosis pathologic morphology and masson to observe collagen content in plaques, Computer image analyzer to measure plaque area, collagen area, vascular cross-sectional area, calculating correction plaque area(plaque area/vascular cross-sectional area)and correction of collagen area(collagen area/ vascular cross-sectional area). Immunohistochemical staining and Western blot analysis of Interleukin 6(IL-6), LP- PLA2 and soluble intercellular adhesion molecule-1(s ICAM-1) expression in plaque.Results1. The serum PON1 activity of coronary heart disease group is significantly lower than the control group(P<0.05); PON1 activity decreased with increasing coronary lesion count(P<0.05); The unstable plaque group was obviously lower than that of PON1 activity in the stable plaque group(P<0.05). LP-PLA2 activity levels in the team significantly higher than the control group(P<0.05);LP-PLA2 activity increased with increasing coronary lesion count(P<0.05);LP-PLA2 activity was positively correlated with total cholesterol and LDL levels.2. Group AS compared with the control group, serum TG, TC, LDL and APOB increased significantly, HDL decreased, serum PON1 activity declined and LP-PLA2 activity increased, ox-HDL and MDA content increased, the patchs IL-6, LP- PLA2 and s ICAM-1 expression increases, the difference had statistical significance(P < 0.05). Serum HDL rose after given coenzyme Q10, increased serum PON1 activity and LP-PLA2 activity decline, serum ox-HDL and MDA decreased. Compared with the AS model group the aorta plaque lesions can alleviate coenzyme Q10 group, collagen content increased(P < 0.05), IL-6, LP-PLA2, s ICAM-1 expression decreased significantly in the aortic(P < 0.05).Coenzyme Q10 can also enhance the positive control medicine the effect of atorvastatin(P < 0.05).Conclusion1. Serum PON1 and LP-PLA2 activity correlated with the incidence of coronary heart disease and coronary artery lesion count; PON1 activity can be used as observation index of coronary plaque stability.2. This study from the pathological morphology observed coenzyme Q10 can reduce the aorta AS degree of pathological changes, increased collagen content and plaque stability. Its mechanism may be related to coenzyme Q10 can increase AS rats serum HDL levels and improve HDL function, reduce oxidative stress levels in rats and the influence of aortic expression of inflammatory markers. |
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