Résumé
Objective To observe the effects of lycopene on fibrinolytic activity and nitric oxide in atherosclerosis rabbits. Methods 30 New Zealand rabbits were randomly divided into three groups. They were individually housed in metal cages. Throughout the experimental period, they were given restricted amounts of food. Control group was fed with normal diet,model group was fed with 1% cholesterol,10% lard and 89% normal diet, lycopene group was fed with 1% cholesterol,10% lard and normal diet plus 6% lycopene.At the time of the first day and the 8th week, blood samples were drawn from ear edge vein of rabbits. The activity and content of plashaa tissue type plasminogen activator(t-PA)and plasminogen activator inhibitor(PAI-1)were detected. The levels of serum Nitric oxide (NO)were determined.At the end of the study, the plaque areas were measured. SPSS 10.0 software was used to evaluate the differences among the three groups. Results Compared with control group, atherosclerosis rabbits had lower content and activity of t-PA, higher content and activity of PAI-1 and lower content of NO. Compared with model group, lycopene group had no significant difference about the content and activity of tPA and PAI-1.But lycopen increased the levels of serum NO, significantly diminished the area of lipid plaque. Conclusions The experimental results suggested that lycopene had antiatherogenic effects. The possible mechanisms might be that lycopene could decrease lipid peroxidation injure, maintain the concentration of NO and protect vascular endothelium. The antiatherogenic effects of lycopene had no correlation with the fibrinolytic activity.
Résumé
Objective To investigate the biological effect of transforming growth factor-?1(TGF-?1) on inducing myofibroblast formation in hypoxic pulmonary vascular remodeling.Methods Forty male Wistar rats were exposed to hypoxia for 0,3,7,14 or 21 days.Mean pulmonary arterial pressure(mPAP),vessel morphometry,right ventricle hypertrophy index(RVHI) were measured.Immunocytochemistry was used to measure the expression of ?-Smooth-muscle actin(?-SMA) and TGF-?1 in pulmonary artery walls and in situ hybridization was used to measure the expression of TGF-?1 mRNA in pulmonary artery walls.Ultrastructure alveolar wall vessels were observed by electron microscopy.Human embryonic lung fibroblasts(KMB17) phenotype after induction of hypoxiaand TGF-?1 were recorded through cell culture.Results(1) mPAP increased significantly after 7-day of hypoxia(P