摘要
目的探讨氧化应激和炎症反应在慢性肾功能衰竭(CRF)患者内皮功能失调和动脉粥样硬化中的作用。方法取63例CRF患者(CRF组,其中非血透组30例,血透组33例)和27例健康对照组外周血,硫代巴比妥酸法测血浆丙二醛(MDA);5’5’-二硫代双2-硝基苯甲酸比色法测血浆谷胱甘肽过氧化物酶活性(GSHPx);应用ELISA法测定TNF-α、超敏C反应蛋白(hs-CRP)、内皮素-1(ET-1)、一氧化氮(NO)及血管性血友病因子(vWF)。结果CRF患者血浆MDA、hs-CRP、TNF-α水平高于健康对照组,GSHPx、NO则低于健康对照组,血液透析加深这种改变;多因素逐步回归分析显示,影响vWF、NO和ET-1的因素有MDA、GSHPx、TNF-α、hs-CRP、Scr(R2分别为0.502,0.631,0.476,P<0.05);影响MDA的因素有TNF-α、hs-CRP(R2=0.709,P<0.05)。结论氧化应激及炎症反应是CRF患者内皮功能紊乱的重要原因之一,氧化应激和炎症反应及其相互作用共同参与了CRF患者内皮功能紊乱和动脉粥样硬化的形成和发展。
Objective To investigate the roles of oxidative stress and inflammatory reaction in pathogenesis of endothelial dysfunction and atherosclerosis in patients with chronic renal failure（CRF）. Methods 63 CRF patients were divided into non-dialysis group and hemodialysis group and 27 healthy volunteers were involved in the study. The levels of plasma malondialdehyde（MDA） were determined by thiobarbituric acid reaction, the activity of glutathione peroxidase（GSHPx） was mearsured by spectrophotometry, plasma nitric oxide（NO）, high-sensitive C-reactive protein （ hs- CRP）, endothelin- 1 （ ET- 1 ） and tumor necrosis factor （TNF） -α were determined by sensitive enzyme-linked imunosorbent assay（ELISA）.Results LeveLs of plasma MDA,hs-CRP,IL-6,TNF-αand ET-1 in CRF patients were higher than those in healthy controls,while NO,GSHPx were lower than those in healthy controls and hemodialysis aggravated these changes. Multivariate stepwise regressive analysis showed that ET- 1, vWF and NO were related to MDA, TNF-α, hs-CRP, Cr （R^2 = 0. 502,0.631,0. 476, respectively, P 〈 0.05 ）. The factors associated with MDA were TNF-α, hs-CRP. Conclusion Oxidative stress and inflammatory reaction are important causes of endothelial dysfunction in CRF patients. Oxidative stress and inflammatory reaction and their interaction may result to endothelial dysfunction and atheroselerosis in CRF patients.
出处
《中国基层医药》
CAS
2006年第4期641-642,共2页
Chinese Journal of Primary Medicine and Pharmacy
关键词
肾功能衰竭
慢性
内皮
血管
氧化性应激
炎症
Kidney failure,chronic
Endothelium,vaseular
Oxidative stress
Inflammation
