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ACS患者体内同型半胱氨酸与黏附分子CD11b/CD18的相关性(PDF)

《心脏杂志》[ISSN:1009-7236/CN:61-1268/R]

期数:
2005年第4期
页码:
365-366
栏目:
临床研究
出版日期:
2005-09-05

文章信息/Info

Title:
The correlation between homocysteine level and CD11b/CD18 expression on leucocytes in the patients with acute coronary syndrome
作者:
杨泉1 郭雪微1 阿祥仁2 徐义先1 谢萍1 施一凡1
1. 兰州医学院附属第三临床医院, 甘肃 兰州 730000; 2. 青海省人民医院
Author(s):
YANG Quan1 GUO Xuewei1 A Xiangren2 XU Yixian1 XIE Ping1 SHI Yifan1
1. Third Hospital of Medical College of Lanzhou, Lanzhou, Gansu 730000, China; 2. People′s Hospital of Qinghai
关键词:
急性冠脉综合征 同型半胱氨酸 白细胞黏附分子
Keywords:
acute coronary syndrome homocysteine CD11b/CD18
分类号:
R543.3
DOI:
-
文献标识码:
A
摘要:
目的 探讨急性冠脉综合征患者体内血浆同型半胱氨酸(HCY)与全血白细胞黏附分子CD11b/CD18水平的变化及其相关性。 方法 对急性冠脉综合征(ACS)患者53例与健康人35例采用酶联免疫法测定血浆HCY水平,通过流式细胞仪采用直接免疫荧光法测定白细胞黏附分子CD11b/CD18的表达。 结果 ACS组血浆HCY水平显著高于对照组,分别为29.1±13.5和12.7±6.9 μmol/L(P<0.01),ACS组白细胞表面CD11b/CD18表达水平显著高于对照组,分别为6.0±2.3比4.3±1.6 MFI(P<0.05),27.7±7.7比19.6±4.9 MFI(P<0.05) 。HCY水平与CD11b、CD18的表达显著相关。结论 同型半胱氨酸作为炎症介质可能通过调节白细胞黏附分子CD11b/CD18的表达,在ACS发生和发展中起重要作用。
Abstract:
AIM To evaluate the plasma homocysteine level and CD11b/CD18 expression on leukocytes in whole blood and their relationship in patients with acute coronary syndrome (ACS). METHODS Our study included 53 patients with ACS and 35 healthy controls based on their clinical situation, electrocardiogram, cardiac enzyme, cTNT and etc. HCY level was measured by enzyme immunoassay and leukocyte surface adhesive molecule CD11b/CD18 expressions were analyzed by immunofluorescence flow cytometry. RESULTS The levels of plasma homocysteine were markedly increased and the expressions of CD11b/CD18 on leucocytes were significantly increased in patients with ACS compared to control group. The correlation between homocysteine level and CD11b/CD18 expression was positive in ACS. CONCLUSION Homocysteine might play an important role in the occurrence of ACS by mediating expression of CD11b/CD18 on leukocyte as an inflammatory medium.

参考文献/References

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备注/Memo

备注/Memo:
收稿日期:2004-09-20.
更新日期/Last Update: 2010-01-05