中国医师进修杂志
中國醫師進脩雜誌
중국의사진수잡지
CHINESE JOURNAL OF POSTGRADUATES OF MEDICINE
2014年
21期
39-42
,共4页
肺栓塞%氧化性应激%DNA损伤
肺栓塞%氧化性應激%DNA損傷
폐전새%양화성응격%DNA손상
Pulmonary embolism%Oxidative stress%DNA damage
目的 探讨急性期及病情缓解后肺血栓栓塞(PE)患者氧化应激状态、外周血单个核细胞(PBMCs)DNA氧化损伤情况.方法 采用单细胞凝胶电泳法(彗星试验)检测35例急性PE患者(试验组)及33例健康体检者(对照组)PBMCs DNA损伤程度;菲罗啉比色法检测血浆总抗氧化能力(TAG);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.结果 试验组病情缓解后血浆TAC、GSH-PX活性均较急性期明显升高[(6.86±1.21) kU/L比(5.18±1.13) kU/L、(165.25 ±41.96) kU/L比(137.23±38.52) kU/L],但均显著低于对照组[(7.85±1.44),(189.92±51.32)kU/L],差异有统计学意义(P＜0.01);试验组病情缓解后血浆MDA含量较急性期明显降低[(5.58±1.89)μmol/L比(7.26±2.25)μmol/L],但均显著高于对照组[(3.71±1.52) μmol/L],差异有统计学意义(P＜0.01).试验组病情缓解后PBMCs DNA损伤程度(29.01±6.75)较急性期(42.13±8.01)明显减轻,但均显著高于对照组(15.12 ±4.36),差异有统计学意义(P＜0.01).试验组病情缓解后及急性期PBMCs DNA损伤均与血浆TAC呈负相关(r=-0.695,P＜0.01;r=-0.536,P＜ 0.01)、与血浆MDA含量呈正相关(r =0.513,P＜0.01;r=0.628,P＜0.01);试验组病情缓解后及急性期血浆TAC均与MDA含量呈负相关(r=-0.534,P＜ 0.01;r=-0.486,P＜0.05)、与GSH-PX活性呈正相关(r=0.512,P＜0.01;r=0.497,P＜ 0.01).结论 PE患者急性期体内氧化/抗氧化失衡,存在氧化应激及其介导的PBMCsDNA损伤;PE患者病情缓解后,氧化应激及其介导的PBMCs DNA损伤减轻.
目的 探討急性期及病情緩解後肺血栓栓塞(PE)患者氧化應激狀態、外週血單箇覈細胞(PBMCs)DNA氧化損傷情況.方法 採用單細胞凝膠電泳法(彗星試驗)檢測35例急性PE患者(試驗組)及33例健康體檢者(對照組)PBMCs DNA損傷程度;菲囉啉比色法檢測血漿總抗氧化能力(TAG);硫代巴比妥痠比色法檢測血漿丙二醛(MDA)含量;改良Hafeman直接測定法(DNTB)檢測血漿穀胱甘肽過氧化物酶(GSH-PX)活力.結果 試驗組病情緩解後血漿TAC、GSH-PX活性均較急性期明顯升高[(6.86±1.21) kU/L比(5.18±1.13) kU/L、(165.25 ±41.96) kU/L比(137.23±38.52) kU/L],但均顯著低于對照組[(7.85±1.44),(189.92±51.32)kU/L],差異有統計學意義(P＜0.01);試驗組病情緩解後血漿MDA含量較急性期明顯降低[(5.58±1.89)μmol/L比(7.26±2.25)μmol/L],但均顯著高于對照組[(3.71±1.52) μmol/L],差異有統計學意義(P＜0.01).試驗組病情緩解後PBMCs DNA損傷程度(29.01±6.75)較急性期(42.13±8.01)明顯減輕,但均顯著高于對照組(15.12 ±4.36),差異有統計學意義(P＜0.01).試驗組病情緩解後及急性期PBMCs DNA損傷均與血漿TAC呈負相關(r=-0.695,P＜0.01;r=-0.536,P＜ 0.01)、與血漿MDA含量呈正相關(r =0.513,P＜0.01;r=0.628,P＜0.01);試驗組病情緩解後及急性期血漿TAC均與MDA含量呈負相關(r=-0.534,P＜ 0.01;r=-0.486,P＜0.05)、與GSH-PX活性呈正相關(r=0.512,P＜0.01;r=0.497,P＜ 0.01).結論 PE患者急性期體內氧化/抗氧化失衡,存在氧化應激及其介導的PBMCsDNA損傷;PE患者病情緩解後,氧化應激及其介導的PBMCs DNA損傷減輕.
목적 탐토급성기급병정완해후폐혈전전새(PE)환자양화응격상태、외주혈단개핵세포(PBMCs)DNA양화손상정황.방법 채용단세포응효전영법(혜성시험)검측35례급성PE환자(시험조)급33례건강체검자(대조조)PBMCs DNA손상정도;비라람비색법검측혈장총항양화능력(TAG);류대파비타산비색법검측혈장병이철(MDA)함량;개량Hafeman직접측정법(DNTB)검측혈장곡광감태과양화물매(GSH-PX)활력.결과 시험조병정완해후혈장TAC、GSH-PX활성균교급성기명현승고[(6.86±1.21) kU/L비(5.18±1.13) kU/L、(165.25 ±41.96) kU/L비(137.23±38.52) kU/L],단균현저저우대조조[(7.85±1.44),(189.92±51.32)kU/L],차이유통계학의의(P＜0.01);시험조병정완해후혈장MDA함량교급성기명현강저[(5.58±1.89)μmol/L비(7.26±2.25)μmol/L],단균현저고우대조조[(3.71±1.52) μmol/L],차이유통계학의의(P＜0.01).시험조병정완해후PBMCs DNA손상정도(29.01±6.75)교급성기(42.13±8.01)명현감경,단균현저고우대조조(15.12 ±4.36),차이유통계학의의(P＜0.01).시험조병정완해후급급성기PBMCs DNA손상균여혈장TAC정부상관(r=-0.695,P＜0.01;r=-0.536,P＜ 0.01)、여혈장MDA함량정정상관(r =0.513,P＜0.01;r=0.628,P＜0.01);시험조병정완해후급급성기혈장TAC균여MDA함량정부상관(r=-0.534,P＜ 0.01;r=-0.486,P＜0.05)、여GSH-PX활성정정상관(r=0.512,P＜0.01;r=0.497,P＜ 0.01).결론 PE환자급성기체내양화/항양화실형,존재양화응격급기개도적PBMCsDNA손상;PE환자병정완해후,양화응격급기개도적PBMCs DNA손상감경.
Objective To explore the level of the oxidative stress and the DNA oxidative damage of peripheral blood mononuclear cells (PBMCs) in pulmonary embolism (PE) patients after remission and in acute exacerbation.Methods The PBMCs DNA damage in 35 PE patients (test group) after remission and in acute exacerbation respectively and in 33 healthy persons (control group) was detected by single-cell gel electrophoresissingle (Comet assay).The total antioxidative capacity (TAC) in blood plasma was measured by phenanthroline colorimetric analysis.The contents of malondialdehyde (MDA) in blood plasma was measured by thiobarbituricacid colorimetric analysis.The capacity of glutathion peroxidase (GSH-PX) in blood plasma was measured by the method of improved Hafeman direct determination method (DNTB).Results The level of TAC,GSH-PX in test group after remission were significantly higher than those in acute exacerbation[(6.86 ± 1.21) kU/L vs.(5.18 ± 1.13) kU/L,(165.25 ± 41.96) kU/L vs.(137.23 ± 38.52) kU/L] (P ＜0.01),and they were all significantly lower than those in control group [(7.85 ± 1.44),(189.92 ± 51.32) kU/L] (P ＜ 0.01).The level of MDA in test group after remission was significantly lower than that in acute exacerbation [(5.58 ± 1.89) μmol/L vs.(7.26 ± 2.25) μmol/L] (P ＜ 0.01),and they were significantly higher than that in control group [(3.71 ± 1.52) μmol/L] (P ＜ 0.01).The arbitrary units (AU) of PBMCs DNA damage in PE patients after remission (29.01 ± 6.75) was significantly lower than that in acute exacerbation (42.13 ± 8.01),and they were all significantly higher than that in control group (15.12 ± 4.36),there were significant differences (P＜ 0.01).There were negative correlations between the PBMCs DNA damage and the level of TAC in PE patients after remission and in acute exacerbation (r =-0.695,P ＜ 0.01 ;r =-0.536,P ＜ 0.01).There were positive correlations between the PBMCs DNA damage and the contents of MDA in PE patients after remission and in acute exacerbation (r =0.513,P ＜ 0.01 ;r =0.628,P ＜ 0.01).There were negative correlations between the level of TAC and the contents of MDA in PE after remission and in acute exacerbation respectively (r =-0.534,P ＜ 0.01 ;r =-0.486,P ＜ 0.05).There were positive correlation between the level of TAC and GSH-PX in PE patients after remission and in acute exacerbation (r =0.512,P ＜ 0.01 ;r =0.497,P ＜ 0.01).Conclusions There are oxidation/antioxidation imbalance,oxidative stress and the PBMCs DNA damage in PE patients.There is positive correlation between the PBMCs DNA damage and the oxidative stress.After remission,the level of the oxidative stress and the PBMCs DNA oxidative damage in the same PE patients is improved respectively.
