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激活蛋白-1在不稳定冠状动脉病变中的作用

The role of activator protein-1 in unstable coronary atherosclerotic changes
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摘要 目的探讨冠心病患者激活蛋白-1与冠状动脉(冠脉)粥样硬化病变的关系。方法根据冠脉造影将142例患者分为冠心病组和对照组。冠心病组根据临床类型、病变类型和病变程度进一步分组。裂解外周血白细胞,测定磷酸化c—Jun吸光度(A),反映活化AP-1数量。结果磷酸化c-Jun A值冠心病组明显高于对照组(1.43±0.33比0.71±0.13,P〈0.001),急性冠脉综合征组明显高于稳定性心绞痛组(1.56±0.28比1.14±0.25,P〈0.001)。磷酸化c-Jun随冠脉病变类型和程度的加重而增加。结论AP-1表达量增高与冠脉粥样硬化发生显著相关,其可能作为预测冠脉粥样硬化病变及斑块稳定性的一个指标。 Objective To investigate the relation between activator protein-1 ( AP-1 ) and coronary atherosclerotic changes and the potential role of AP-1 in the stabilization of atherosclerotic plaques in patients with coronary heart disease (CHD). Method 142 patients were included in this study and divided into CHD group( 107 ) and control group (35) according to coronary angiography (CAG). The CHD group was further divided into a stable angina pectoris (SAP) group (32) and an acute coronary syndrome (ACS) group (75) according to the clinical manifestations, In addition, the CHD group was divided into A type group, B type group and C type group according to the standard of ACC/AHA coronary change in 1988. Meanwhile, the CHD group was further divided into light stenosis group, moderate stenosis group and severe stenosis group according to the degree of coronary lesion. The lysate of cells was obtained through lysis of the leucocyts from peripheral blood with cell lysis buffer. The amount of Phospho-c-Jun in lysate was measured with enzyme-linked immunosorbent assay (ELISA). The results were demonstrated with absorbance, which reflects the amount of AP-1. Results The main coronary changes in the SAP group were A type (68. 7% ) and the changes were mainly of light degree (53. 1% ) ; the main coronary changes in the ACS group were B type( 52. 0%) or C type (37. 3%) and the changes were mainly of heavy degree (66. 7%). The absorbance of Phospho-c-Jun in CHD group was significantly higher than that in the control subjects ( 1.43 ± 0. 33 vs 0. 71 ±0. 13, P 〈 0. 001 ). The absorbance of Phospho-c-Jun in the ACS group was significantly higher than that in the SAP group ( 1.56 ±0. 28 vs 1.14 ±0. 25, P 〈0. 001 ). The absorbance of Phospho- c-Jun increased gradually from A type group to C type group ( 1.18 ±0. 27 vs 1.42 ±0. 26 vs 1.71 ±0. 27, P 〈0. 001 ) and from light stenosis group to severe stenosis group ( 1.09 ±0. 20 vs 1.37 ±0. 26 vs 1.60 ± 0. 29, P 〈 0.001 ). Conclusion There is a significant relationship between AP-1 and coronary atherosclerotic changes. AP-1 may be a factor that can predict coronary arteriosclerotic progression and stability of the plaque.
出处 《中华内科杂志》 CAS CSCD 北大核心 2008年第7期545-547,共3页 Chinese Journal of Internal Medicine
基金 成都军区医学科研“十一五”计划A类课题(MA07010)
关键词 冠状动脉疾病 冠状动脉硬化 激活蛋白-1 Coronary disease Coronary atherosclerosis Activator protein-1
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  • 1Surh YJ, Na HK, Lee SS. Transcription factors and mitogenactivated protein kinases as molecular targets for chemoprevention with anti-inflammatory phytochemicals. Biofactors, 2004,21 : 103- 108.
  • 2Lin SJ, Shyue SK, Hung YY, et al. Supemxide dismutase inhibits the expression of vascular cell adhesion molecule-1 and intracellular cell adhesion molecule-1 induced by tumor necrosis factor-alpha in human endothelial ceils through the JNK/p38 pathways. Arterioscler Thromb Vasc Biol,2005 ,25 :334-340.
  • 3VernaL, Ganda C, Stemerman MB. In vivo low-density lipoprotein exposure induces intercellular adhesion molecule-1 and vascular cell adhesion molecule-1 correlated with activator protein- 1 expression. Arterioscler Thromb Vasc Biol,2006,26 : 1344-1349.
  • 4Cullen JP, Morrow D, Jin Y, et al. Resveratrol, a polyphenolie phytostilbene, inhibits endothelial monocyte chemotactic protein-1 synthesis and secretion. J Vasc Res ,2007,44:75-84.
  • 5LiL, Sawamura T, Renier G. Glucose enhances human macrophage LOX-1 expression: role for LOX-1 in glucose-induced macrophage foam cell formation. Circ Res, 2004,94:892-901.
  • 6Chandrasekar B, Mummidi S, Mahimainathan L, et al. Intedeukin-18-induced human coronary artery smooth muscle cell migration is dependent on NF-kappaB-and AP-1-mediated matrix metalloproteinase-9 expression and is inhibited by atorvastatin. J Biol Chem,2006,281:15099-15109.
  • 7Lee J, Jung E, Lee J, et al. Emodin inhibits TNF alpha-induced MMP-1 expression through suppression of activator protein-1 ( AP- 1 ). Life Sci ,2006,79:2480-2485.
  • 8Bea F,Kreuzer J, Preusch M,et al. Melagatran reduces advanced atherosclerotic lesion size and may promote plaque stability in apolipoprotein E-deficient mice. Arterioscler Thromb Vasc Biol, 2006,26:2787-2792.

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