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氧化还原态失衡与冠状动脉粥样硬化性心脏病
引用本文:黄彦生,王丽霞,王光公.氧化还原态失衡与冠状动脉粥样硬化性心脏病[J].临床荟萃,2009,24(19):1694-1697.
作者姓名:黄彦生  王丽霞  王光公
作者单位:河南省人民医院心内科,河南,郑州,450003
基金项目:河南省医学科技攻关计划项目
摘    要:目的探讨氧化还原态失衡与冠状动脉粥样硬化性心脏病(冠心病)的关系。方法根据冠状动脉造影结果,将123例疑似冠心病住院患者分为冠心病组(A组)41例,冠状动脉粥样硬化组(B组)45例,冠状动脉正常组(C组)37例。取所有研究对象静脉血,测血浆还原型谷胱甘肽(GSH)与氧化型谷胱甘肽(GSSG),氧化型低密度脂蛋白(oxLDL)和丙二醛(MDA)浓度。计算GSH/GSSG氧化还原电位,与冠状动脉斑块积分及oxLDL行相关性分析。结果随冠状动脉斑块积分增高(从C组-A组),GSH、GSH/GSSG逐次减低,分别为(321.27±56.89)μmol/L,(309.52±44.56)μmol/L,(285.71±38.23)μmol/L(P〈O.05);10.56±1.70,9.86±1.58,8.65±1.18(P〈0.05);GSSG、GSH/GSSG氧化还原电位逐次升高,分别为(30.42±1.53)μmol/L,(31.39±1.64)μmol/L,(33.03±1.75)μmol/L(P〈0.05);(-142.39±1.33)mV,(-140.18±1.12)mV,(-136.17±1.01)mV(P〈0.05);氧化应激损伤产物oxLDI、MDA亦随冠状动脉斑块积分增高而增加,分别为(417.22±126.61)μg/L,(557.24±171.83)μg/L,(691.96±203.55)μg/L(P〈0.05);(2.39±1.24)μmol/L,(3.25±1.37)μmol/L,(4.39±1.52)μmol/L(P〈0.05);GSH/GSSG氧化还原电位与oxLDL呈明显正相关(r=0.823,P〈0.001)。结论随着冠状动脉斑块积分增高,血浆GSH/GSSG氧化还原态向氧化方向明显偏移,这可能与动脉粥样硬化的发生发展有关。

关 键 词:冠状动脉疾病  谷胱甘肽  脂蛋白类  LDL

Redox status imbalance in coronary atherosclerotic cardiopathy
HUANG Yan-sheng,WANG Li-xia,WANG Guang-gong.Redox status imbalance in coronary atherosclerotic cardiopathy[J].Clinical Focus,2009,24(19):1694-1697.
Authors:HUANG Yan-sheng  WANG Li-xia  WANG Guang-gong
Institution:(Department of Cardiology, Henan Provincial People's Hospital, Zhengzhou 450003, China)
Abstract:Objective To explore the relationship between redox status imbalance and coronary atheroselerotic cardiopathy(CAD). Methods 123 patients who might be CAD and hospitalized were divided into three groups by the results of coronary arteriography. 41 patients fell into coronary atherosclerotic eardiopathy group (group A),45 cases coronary atherosclerosis group (group B) ,and 37 cases coronary normal group (group C). All patients had their plasma glutathione (reduced form GSH and oxidized form GSSG), oxidized low density lipoprotein (oxLDL) and malondialdehyde (MDA) been measured. The GSH/GSSG redox potential was calculated according to Nernst equation, and their correlation with coronary atherosclerotic plaque integral and oxLDL was analyzed. Results Along with the coronary atherosclerotic plaque integral increasing (from group C to group A), GSH and GSH/GSSG gradually reduced, respectively ( 321.27 ± 56.89 ) μmol/L, ( 309. 52± 44.56 ) μmol/L, ( 285.71 ± 38. 23 ) μmol/L ( P % 0.05 ) ; 10.56 ±1.70,9.86 ±1.58,8.65 ± 1.18 ( P 〈 0.05), and GSSG and GSH/GSSG redox potential gradually increased, respectively (30.42±1.53) μmol/L, (31. 39±1. 64) μmol/L, (33. 03±1.75) μmol/L( P〈0.05) ;(-142.39±1.33) mV ,(-140.18±1.12) mV,(-136.17 ± 1.01) mV( P 〈0.05). The products of oxidative stress oxLDL and MDA also increased significantly,respectively (417.22 ± 126.61 ) μg/L, (557.24 ± 171.83 ) μg/L, (691. 96 ± 203.55) μg/L (P〈0.05);(2.39±1.24) μmol/L,(3.25±1.37) μmol/L, (4. 39 ±1. 52) μmol/L(P 〈0.05). The analysis for relationship between GSH/GSSG redox potential and oxLDL showed Mgnificant and positive correlations ( r= 0. 823, P〈0. 001). Conclusion GSH/GSSG redox status shifts to oxidizing direction along with the coronary atherosclerotie plaque integral increasing. It may be implicated in the atherosclerosis generating and progressing.
Keywords:LDL
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