CAJ | 학술논문

目的观察番茄红素对高脂喂饲所致动脉粥样硬化兔模型内源性纤溶活性及一氧化氮的影响.方法采用高脂喂饲模型,将30只新西兰家兔随机分为3组:对照组、高脂模型组和番茄红素组,分别给予普通饲料(正常对照组)和高脂饲料(其它2组)喂养,番茄红素组另加用番茄红素;于实验开始前1 d和开始后第8周末取空腹血测定血浆t-PA、PAI-1活性和含量以及血清一氧化氮含量.实验结束后,观察主动脉血管病理变化.结果与正常对照组相比,高脂模型组t-PA活性与含量减低,PAI-1活性与含量增加,NO含量减低;与高脂模型组相比,番茄红素组t-PA、PAI-1活性与含量差异无统计学意义;但一氧化氮含量增加(t=2.05,P＜0.05),主动脉脂质斑块面积减少(t=1.94,P＜0.05).结论动脉粥样硬化兔纤溶活性减低,番茄红素对动脉粥样硬化病变形成具有较好的保护作用.其保护作用与改善内源性纤溶活性无关;与抗氧化损伤,维持一氧化氮分泌,保护血管内皮功能有关.
목적 관찰번가홍소대고지위사소치동맥죽양경화토모형내원성섬용활성급일양화담적영향.방법 채용고지위사모형,장30지신서란가토수궤분위3조:대조조、고지모형조화번가홍소조,분별급여보통사료(정상대조조)화고지사료(기타2조)위양,번가홍소조령가용번가홍소;우실험개시전1 d화개시후제8주말취공복혈측정혈장t-PA、PAI-1활성화함량이급혈청일양화담함량.실험결속후,관찰주동맥혈관병리변화.결과 여정상대조조상비,고지모형조t-PA활성여함량감저,PAI-1활성여함량증가,NO함량감저;여고지모형조상비,번가홍소조t-PA、PAI-1활성여함량차이무통계학의의;단일양화담함량증가(t=2.05,P＜0.05),주동맥지질반괴면적감소(t=1.94,P＜0.05).결론 동맥죽양경화토섬용활성감저,번가홍소대동맥죽양경화병변형성구유교호적보호작용.기보호작용여개선내원성섬용활성무관;여항양화손상,유지일양화담분비,보호혈관내피공능유관.
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.