摘要
目的 :多年来对尿酸 (UA)浓度增高是否为冠心病的独立危险因素一直存在争论。虽有证据表明高浓度UA对血管内膜、内皮细胞、局部缺血缺氧组织等有损害作用 ,但确切的机制尚未十分明了。本文通过检测不同浓度UA对体外培养的人脐静脉内皮细胞株 (ECV30 4 )脂质过氧化产物 (H2 O2 、MDA)、肿瘤坏死因子α(TNF -α)水平的影响 ,探讨UA在动脉粥样化 (AS)发生发展中的可能机制 ,并观察高浓度胰岛素 (Ins)对之有无协同损伤作用。结果 :1 不同浓度UA对脂质过氧化代谢表现双向效应 ,低浓度可减弱 ,高浓度促进脂质过氧化物的产生并呈浓度依赖关系 ;高浓度增加TNF -α的分泌 ;2 Ins对于高浓度UA状态下的脂质过氧化具有协同损害作用 ,低浓度状态下作用不明显 ;3 未观察到Ins对TNF -α产生的明显影响。上述结果提示 :生理浓度下UA具有抗氧化效应 ,过高浓度则会增加血管内皮细胞脂质过氧化物和炎症介质的产生 。
Objective:Although it has been debated for many years,the problem of whether uric acid is an independent risk factor of cardiovascular disease is not understood clearly.There are few evidence that high UA could injure intima of vessel,endothelial cell and ischemia or hypoxia constitution,but the certain mechanism is not distinct.The purpose of this study is to discuss the possible mechanism of UA in arteriosclerosis(AS),meanwhile to observe if high insulin(Ins)could synergetically injure endothelial cells.Method:UA in different concentration(0,5,15,30mg/dL)with or without Ins were added into the medium of cultured endothelial cells and incubated for 24,48,72 hours respectively.Lipid peroxidation and tumor necrosis factor-alpha(TNF-α)were assessed.Results:(1).UA in different concentration have opposite manifestation to lipid peroxidation,low UA weakening while high UA facilitating.High UA could increase excretion of TNF-α too.(2)Insulin aggravate the peroxidation effect of UA,while have no distinct effect on TNF-α.Conclusion:UA in physiological concentration may have anti-peroxidation effect and in high concentration would add the stress of lipid peroxidation as well as increase inflammatory medium content.High UA may be involved in AS by above-mentioned mechanism.
出处
《华西医学》
CAS
2004年第3期417-419,共3页
West China Medical Journal
