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慢性阻塞性肺疾病患者氧化应激和病情变化的研究 被引量:6

Oxidative stress and change of pathogenetic condition in COPD patients
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摘要 目的探讨慢性阻塞性肺疾病(COPD)患者急性加重期及病情缓解后氧化应激程度。方法选取33例慢性阻塞性肺疾病急性加重期(AECOPD)患者(实验组)及31例健康体检者(对照组)采用菲罗啉比色法检测血浆总抗氧化能力(TAC)、硫代巴比妥酸比色法检测血浆丙二醛(MDA)含量、改良Hafeman直接测定法(DNTB)检测血浆谷胱甘肽过氧化物酶(GSH-PX)活力,同时进行动脉血气检测及功能性呼吸困难评分。结果实验组病情缓解后动脉血氧分压(PaO2)(62.32±8.50)mmHg(1 mmHg=0.133 kPa)较急性加重期(49.06±7.64)mmHg升高(P<0.01);动脉血二氧化碳分压(PaCO2)(41.81±7.23)mmHg较急性加重期(45.63±7.81)mmHg降低(P<0.05)。实验组病情缓解后功能性呼吸困难评分(MMRC)(1.55±0.61)较急性加重期(2.61±0.68)显著好转(P<0.01)。实验组病情缓解后血浆TAC、GSH-PX均较急性加重期明显升高(6.77±1.28)kU/L vs(5.52±1.15)kU/L、(168.17±43.66)kU/L vs(132.27±39.45)kU/L明显升高(P<0.01),但显著低于对照组(7.76±1.41)kU/L、(197.92±53.28)kU/L(均P<0.01)。实验组病情缓解后血浆MDA(5.43±1.86)μmol/L较急性加重期(7.28±2.03)μmol/L明显降低(P<0.01),但显著高于对照组(3.89±1.46)μmol/L(均P<0.01)。实验组急性加重期及病情缓解后血浆TAC均与MDA呈负相关(r=-0.587、r=-0.450,P<0.01或<0.05)。实验组急性加重期及病情缓解后血浆TAC均与GSH-PX及PaO2呈正相关(r分别0.556、0.583和0.433、0.396,均P<0.05或<0.01)。实验组急性加重期及病情缓解后血浆TAC与PaCO2无明显相关(r分别为0.230、-0.225,均P>0.05);实验组急性加重期及病情缓解后血浆MDA与PaO2呈负相关(r分别为-0.463、-0.411,均P<0.05)、与PaCO2无明显相关(r分别为0.198、-0.232,均P>0.05)。结论 AECOPD患者体内氧化/抗氧化失衡,存在氧化应激;AECOPD患者加重缓解后,氧化应激损伤明显减轻;AECOPD患者氧化损伤与缺氧密切相关。 Objective To explore the levels of the oxidative stress in chronic obstructive pulmonary disease(COPD) patients in acute exacerbation(AECOPD) and after remission.Methods The total antioxidative capacity(TAC) in blood plasma of 33 patients with COPD in acute exacerbation after remission and respectively and in 31 healthy persons were measured by o-phenanthroline colorimetric analysis.The contents of malondialdehyde(MDA) in blood plasma were measured by thiobarbituricacid colorimetric analysis.The capacity of glutathion peroxidase(GSH-PX) in blood plasma was measured by the method of DNTB.The respiratory functions were measured by arterial blood gas testing and modified medical research council dyspnea scale respectively.Results The indexes associated with respiratory function:the level of PaO2 in AECOPD patients after remission(62.32±8.50) mmHg was higher than than in acute exacerbation(49.06±7.64) mmHg(P0.01),the level of PaCO2 in AECOPD patients after remission(41.81±7.23) mmHg was lower than that in acute exacerbation(45.63±7.81) mmHg(P0.05).The dyspnea scale in AECOPD patients after remission(1.55±0.61) was lower than that in acute exacerbation(2.61±0.68)(P0.01).The degree of oxidative stress:the level of TAC in the blood plasma in AECOPD patients after remission(6.77±1.28) kU/L was significantly higher than that in acute exacerbation(5.52±1.15) kU/L(P0.01),and they were all significantly lower than that in the healthy controls(7.76±1.41) kU/L(all P0.01) respectively.The content of MDA in the blood plasma in AECOPD patients after remission(5.43±1.86) μmol/L was significantly lower than that in acute exacerbation(7.28±2.03) μmol/L(P0.01),and they were all significantly higher than those in the healthy controls(3.89±1.46) μmol/L(all P0.01) respectively.The level of GSH-PX in the blood plasma in AECOPD patients after remission(168.17±43.66) kU/L was significantly higher than that in acute exacerbation(132.27±39.45) kU/L(P0.01),and they were all significantly lower than that in the healthy controls(197.92±53.28) kU/L(all P0.01) respectively.The correlations:there were negative correlations between the levels of TAC and the contents of MDA in AECOPD patients in acute exacerbation and after remission respectively(r=-0.587,P0.01,r=-0.450,P0.05).There were positive correlations between the levels of TAC and GSH-PX in AECOPD patients in acute exacerbation and after remission(respectively r=0.556,0.583,all P0.01).There were positive correlations between the TAC and PaO2 in AECOPD patients in acute exacerbation and after remission(respectively r=0.433,0.396,all P0.05),but there were no correlations between the TAC and PaCO2(respectively r=0.230,-0.225,all P0.05).There were negative correlations between the MDA and PaO2 in AECOPD patients in acute exacerbation and after remission(respectively r=-0.463,-0.411,all P0.05),but there were no correlations between the MDA and PaCO2(respectively r=0.198,-0.232,all P0.05).Conclusion There were oxidation/antioxidation imbalance and oxidative stress in AECOPD patients.There were positive correlations between the oxidative damage and hypoxia.After remission,the levels of the oxidative stress in the same AECOPD patients were significantly improved respectively.
出处 《临床荟萃》 CAS 2010年第21期1874-1877,共4页 Clinical Focus
关键词 肺疾病 慢性阻塞性 丙二醛 谷胱甘肽过氧化物酶 血气监测 经皮 pulmonary disease chronic obstructive malondialdehyde glutathion peroxidase blood gas monitoring transcutaneous
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参考文献15

  • 1Tomaki M,Sugiura H,Koarai A,et al. Decreased expression of antioxidant enzymes and increased expression of chemokines in COPD[J]. Pulm Pharmacol Ther, 2007,20 (5): 596-605.
  • 2慢性阻塞性肺疾病诊治指南(2007年修订版)[J].中华结核和呼吸杂志,2007,30(1):8-17. 被引量:8229
  • 3Hashimoto K, Takasaki W, Yamoto T, et al. Effect of glutaihione (GSH) depletion on DNA damage and blood chemistry in aged and young rats[J]. J Toxicol Sci,2008,33 (4):421-429.
  • 4刘卫,刘晓菊,余勤,赵晋,雷泽林,李龙.结核性胸膜炎患者DNA氧化损伤和脂质过氧化的研究[J].中华结核和呼吸杂志,2003,26(12):781-784. 被引量:12
  • 5Liu XJ,Zhao J,Zheng RE. DNA damage of tumor-associated lymphocytes and total antioxidant capacity in cancerous patients[J]. Murat Res,2003,539(1/2) :1-8.
  • 6姜忠,汤旭磊.白藜芦醇对2型糖尿病患者外周血单个核细胞DNA损伤的体外修复[J].中国临床药理学与治疗学,2006,11(11):1285-1290. 被引量:6
  • 7Mak JC. Pathogenesis of COPD. Part Ⅱ. Oxidative- antioxidative imbalance[J]. Int J Tuberc Lung Dis, 2008, 12 (4) :368-374.
  • 8Augustyniak A,Skrzydlewska E. Antioxidative abilities during aging[J]. Postepy Hig Med Dosw,2004,58:194-201.
  • 9Gerard MT. Proteases in COPD[J]. Chest,2007,132(2) :1724- 1725.
  • 10Chen ZH, Kim HP, Sciurba FC, et al. Egr-1 regulates autophagy in cigarette smoke inducedchronic obstructive pulmonary disease[J]. PLoS ONE, 2008,3(10) : e3316.

二级参考文献31

  • 1钟永,陈平,赵烈炎.浸润型肺结核病人脂质过氧化损伤的研究[J].中国防痨杂志,1995,17(3):125-126. 被引量:1
  • 2有创-无创序贯机械通气多中心研究协作组.以肺部感染控制窗为切换点行有创与无创序贯机械通气治疗慢性阻塞性肺疾病所致严重呼吸衰竭的随机对照研究[J].中华结核和呼吸杂志,2006,29(1):14-18. 被引量:279
  • 3[1]Dincer Y,Akcay T,Ilkova H,Alademir Z,Ozbay G.DNA damage and antioxidant defense in peripheral leukocytes of patients with Type I diabetes mellitus[J].Mutat Res,2003;527:49-55
  • 4[2]Suzuki S,Hinokio Y,Komatu K,Ohtomo M,Onoda M,Hirai S,et al.Oxidative damage to mitochondrial DNA and its relationship to diabetic complications[J].Diabetes Res Clin Pract,1999;45:189-91
  • 5[3]Leonard S S,Xia C,Jiang BH,Stinefelt B,Klandorf H,Harris G K,et al.Resveratrol scavenges reactive oxygen species and effects radical-induced cellular responses[J].Biochem Biophys Res Commun,2003;309:1017-26
  • 6[4]Singh N P,Mccoy MT,Tice RR.A simple technique for low levels of DNA damage in individual cells[J].Exp Cell Res,1988;175:184-91
  • 7[5]King GL,Loeken MR.Hyperglycemia-induced oxidative stress in diabetic complications[J].Histochem Cell Boil,2004;122:333-8
  • 8[6]Rojas A,Morales MA.Advanced glycation and endothelial functions:a link towards vascular complication in diabetes[J].Life sciences,2004;76:715-30
  • 9[7]Sakai K,Matsumoto K,Nishikawa T,Suefuji M,Nakamaru K,Hirashima Y,et al.Mitochondrial reactive oxygen species reduce by pancreatic β-cells[J].Biochem Biophys Res Commun,2003;300:216-22
  • 10[8]Rorbertson RP.Chronic oxidative stress as a central mechanism for glucose toxicity in pancreatic islet beta cells in diabetes[J].J Biol Chem,2004;279:42351-4

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