不同尿酸浓度与氧化应激和内皮损伤指标研究

目的 观察不同血尿酸浓度下氧化应激指标变化,探讨高尿酸引起血管内皮功能损伤的机制.方法 选择男性正常血尿酸及高尿酸血症病例,根据血尿酸值分为5组,每组50例左右,分别测定血浆丙二醛(MDA)、超氧化物歧化酶(SOD)、谷胱甘肽过氧化物酶(GSH·Px)、NO、纤溶酶原激活抑制剂-1(PAI-1)、内皮素-1(ET-1)及各项生化指标.结果 尿酸≥380 μmol/L时,MDA、SOD、GSH-Px、PM-1、ET-1均明显增加,NO明显下降(P值均<0.05),但当尿酸≥420 μmol/L时,SOD、GSH-Px明显下降;回归分析显示PAI-1与MDA、尿酸、HOMA胰岛素抵抗指数(HOMA-IR)、TG正相关,与SOD、NO负相关(t=-3.64～6.08,P<0.05);ET-1与MDA、尿酸、HOMA-IR正相关,与NO、GSH-Px、SOD负相关(t=-4.75～6.35,P<0.05).结论 男性血尿酸超过380 umol/L时引起氧化应激,氧化应激、血尿酸、胰岛素抵抗参与了内皮功能紊乱的形成.

Oxidative stress and endothelial dysfunction at different serum uric acid levels

Objective To investigate the state of oxidative stress in the subjects with different levels of serum uric acid and to explore the cause of endothelial dysfunction induced by hyperuricemia. Methods Male subjects with normal serum uric acid or hyperuricemia were enrolled in this study. According to the levels of serum uric acid,all the partieipante were divided into five groups. Every group consisted of about fifty subjects. Plasma malondialdehyde (MDA), superoxide dismutase (SOD) and glutathione peroxidase(GSH-Px) were determined. In the mean time plasma nitric oxide(NO) ,plasminogen activator inhihitor-1(PAI-1), endothelin-1 (ET-1) and other biochemical variables were also determined. Results When the serum uric acid level was more than 380 μmol/L, the levels of plasma MDA,SOD,GSH-Px, PAI-1 and ET-1 became higher, while the level NO became lower(P<0.05). However SOD and GSH-Px became much lower when the serum uric acid level was more than 420 μmol/L. Multivariate stepwise regressive analysis showed that PAI-1 was positively related to MDA,UA,HOMA-IR and TG, but negatively related to SOD and NO(t =-3.64 - 6. 08,P < 0.05). ET-1 was positively related to MDA, UA, HOMA-IR and negatively related to NO, GSH-Px and SOD (t = - 4.75 - 6.35,P < 0.05 ). Conclusions It is indicated that oxidative stress became much obvious when the serum uric acid level was more than 380 μmol/L . Oxidative stress,high serum uric acid level and insulin resistance may result in endothelial dysfunction.