我们的网站为什么显示成这样?

可能因为您的浏览器不支持样式,您可以更新您的浏览器到最新版本,以获取对此功能的支持,访问下面的网站,获取关于浏览器的信息:

|本期目录/Table of Contents|

冠心病患者激活蛋白-1和脂联素与冠状动脉病变的关系

《心脏杂志》[ISSN:1009-7236/CN:61-1268/R]

期数:
2009年第5期
页码:
669-671,674
栏目:
临床研究
出版日期:
2009-07-14

文章信息/Info

Title:
Relationship of activator protein-1 and adiponectin and coronary atherosclerosis in patients with coronary heart disease
作者:
杨丽霞苗贵华齐峰王先梅石燕昆任丽李明秋
成都军区昆明总医院心血管内科,云南 昆明 650032
Author(s):
YANG Li-xia MIAO Gui-hua QI Feng WANG Xian-mei SHI Yan-kun REN Li LI Ming-qiu
Department of Cardiology, Kunming General Hospital, Chengdu Military Area Command, Kunming 650032, Yunnan, China
关键词:
激活蛋白-1脂联素冠状动脉疾病动脉粥样硬化
Keywords:
activator protein-1 adiponectin coronary disease atherosclerosis
分类号:
R541.4
DOI:
-
文献标识码:
A
摘要:
目的: 探讨冠心病(CHD)患者外周血白细胞内激活蛋白-1(AP-1)和血浆脂联素浓度与CHD及冠状动脉粥样硬化病变的关系。方法: 冠状动脉造影患者142例,分为CHD组和对照组。CHD组根据临床类型分为稳定型心绞痛(SAP)和急性冠脉综合征(ACS)组;根据冠状动脉病变类型分为A,B和C型病变组;根据冠状动脉病变狭窄程度分为轻、中和重度病变组。用ELISA法测定外周血白细胞裂解液中磷酸化c-Jun吸光度(A),反映活化AP-1数量;血浆脂联素浓度通过ELISA法测定。结果: CHD组磷酸化c-Jun明显高于对照组(1.43±0.33 vs 0.71±0.13, P<0.01),脂联素明显低于对照组[(6.1±1.8) mg/L vs (10.2±1.5) mg/L, P<0.01];ACS组磷酸化c-Jun明显高于SAP组(1.56±0.28 vs 1.14±0.25, P<0.01) ,脂联素明显低于SAP组[(5.4±1.5) mg/L vs (7.6±1.7) mg/L, P<0.01]。随冠状动脉病变类型和病变程度的加重,磷酸化c-Jun逐渐升高,脂联素逐渐降低。脂联素浓度与冠脉Gensini评分呈负相关(P<0.05)。结论: 磷酸化c-Jun表达量增高和血浆脂联素浓度降低与CHD类型及冠脉病变情况显著相关。
Abstract:
AIM: To investigate the relation between plasma adiponectin concentration and activator protein-1 (AP-1) in peripheral blood and coronary heart disease (CHD) and coronary arteriosclerosis changes in patients with CHD. METHODS: One hundred and forty-two patients were divided into CHD group and control group according to the outcome of coronary angiography (CAG). CHD group was further divided into stable angina pectoris (SAP) group and acute coronary syndrome (ACS) group according to clinical diagnosis. According to the type of coronary changes, CHD group was divided into type A, type B and type C groups and according to the degree of coronary lesion, CHD group was further divided into light stenosis group, moderate stenosis group and severe stenosis group. Phospho-c-Jun in lysate and plasma adiponectin concentrations were measured by enzyme-linked immunosorbent assay (ELISA). RESULTS: Absorbance of Phospho-c-Jun in the CHD group was significantly higher than in control subjects (1.43±0.33 vs.0.71±0.13, P<0.01). Plasma adiponectin concentration in the CHD group was significantly lower than in control subjects [(6.1±1.8)mg/L vs.(10.2±1.5)mg/L, P<0.01]. Absorbance of Phospho-c-Jun in ACS group was significantly higher than in the SAP group (1.56±0.28 vs.1.14±0.25, P<0.01). Plasma adiponectin concentration in the ACS group was significantly lower than in the SAP group [(5.4±1.5)mg/L vs.(7.6±1.7)mg/L, P<0.01]. Absorbance of Phospho-c-Jun increased gradually from type A group to type C group and from light stenosis group to severe stenosis group. Plasma adiponectin concentration decreased gradually from type A group to type C group and from light stenosis group to severe stenosis group. CONCLUSION: Increase of Phospho-c-Jun (AP-1) and decrease of adiponectin are significantly related to CHD and coronary atherosclerosis changes.

参考文献/References

[1] Lewicki M, Kotyla P, Jankiewicz-Ziobro K, et al. [The role of adiponectin in atherosclerosis][J]. Pol Merkur Lekarski, 2006, 20(118):494-496.

[2] Lin SJ, Shyue SK, Hung YY, et al. Superoxide 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 cells through the JNK/p38 pathways[J]. Arterioscler Thromb Vasc Biol, 2005, 25(2):334-340.

[3] Verna L, 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[J]. Arterioscler Thromb Vasc Biol, 2006, 26(6):1344-1349.

[4] Cullen JP, Morrow D, Jin Y, et al. Resveratrol, a polyphenolic phytostilbene, inhibits endothelial monocyte chemotactic protein-1 synthesis and secretion[J]. J Vasc Res, 2007, 44(1):75-84.

[5] Li CJ, Sun HW, Zhu FL, et al. Local adiponectin treatment reduces atherosclerotic plaque size in rabbits[J]. J Endocrinol, 2007,193(1):137-145.

[6] Chandrasekar B, Mummidi S, Mahimainathan L, et al. Interleukin-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]. J Biol Chem, 2006, 281(22):15099-15109.

[7] Lee J, Jung E, Lee J, et al. Emodin inhibits TNF alpha-induced MMP-1 expression through suppression of activator protein-1(AP-1) [J]. Life Sci, 2006, 79(26):2480-2485.

[8] Kato H, Kashiwagi H, Shiraga M, et al. Adiponectin acts as an endogenous antithrombotic factor[J]. Arterioscler Thromb Vasc Biol, 2006, 26(1):224-230.

[9] Matsuda M, Shimomura I, Sata M, et al. Role of adiponectin in preventing vascular stenosis[J]. J Biol Chem, 2002, 277(40):37487-37491.

备注/Memo

备注/Memo:
收稿日期:2008-6-20.作者简介:杨丽霞,主任医师,博士,主要从事冠心病的介入诊治Email:doctorylixia@yahoo.com.cn
更新日期/Last Update: 2009-07-22