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高脂血症患者粘附分子水平及调脂干预的研究 被引量:2

Changes of plasma adhesion molecules levels and interventions for lipid regulation in patients with hyperlipide-mia
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摘要 目的 观察高脂血症患者可溶性 P-选择素 ( s P- sel)和可溶性细胞间粘附分子 - 1( s ICAM- 1)的表达及阿托伐他汀的调脂干预的作用。方法 用酶联免疫吸附法 ( EL ISA)及放免法检测 32例高脂血症患者 (男 19例 ,女 13例 )服用阿托伐他汀 ( 10 mg/ d,疗程 4~ 6周 )前后血浆 s ICAM- 1和 s P- sel的水平并与性别、年龄相匹配的 30例正常血脂组对照。结果 高脂血症患者血浆 s ICAM- 1和 s P- sel的水平明显高于对照组 ( P<0 .0 1) ;阿托伐他汀治疗 4~ 6周后总胆固醇 ( TC)、甘油三酯 ( TG)、低密度脂蛋白胆固醇 ( L DL - C)、s ICAM- 1和 s P- sel的水平显著下降 ( P<0 .0 1) ;s ICAM- 1和 s P- sel与 TC、L DL- C、TG呈正相关 ( P<0 .0 5 ) ,HDL- C升高不明显。结论  1)血浆 s ICAM- 1和s P- sel的表达增加推测是高脂血症致动脉粥样硬化的一个重要环节 ;2 )阿托伐他汀降低 s ICAM- 1和 s P- sel水平可能主要是通过调节血脂而产生。 Objective To investigate the expression of plasma intercellular adhesion molecule-1,sP-selectin and the effects of atorvastatin intervention lipid lowering in the patients with hyperlipidemia. Methods 32 patients with hyperlipidemia and 30 sex-and age-matched healthy controls were studied; The plasma sP-selectin and sICAM-1 were measured by immunoradiometry and enzyme-linked immunosorbent assay (ELISA) before and after treatment with atorvastatin (10mg/d for 4~6 week) in 32 patients with hyperlipidemia and 30 healthy controls. Results (1) The patients with hyperlipidemia had higher (P<0.01) levels of plasma sP-selectin and sICAM-1 compared with those of control subjects. (2) Administration of atorvastatin to patients with hyperlipidemia significantly reduced plasma LDLC (P<0.01). but HDL-C was not significantly elevated.(3)A direct positive correlation was observed between plasma sP-selection,sICAM-1 levels and TC,TG,LDL-C(P<0.05).
出处 《中国心血管杂志》 2004年第2期121-122,125,共3页 Chinese Journal of Cardiovascular Medicine
关键词 阿托伐他汀 高脂血症 P-选择素 细胞间粘附分子-1 Hyperlipidemia Atorvastatin Intercellular adhesion molecule-1 sP-selectin
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参考文献7

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同被引文献15

  • 1朱彦琪,孙宝贵.可溶性细胞间粘附分子和可溶性血管细胞粘附分子与动脉粥样硬化[J].中国动脉硬化杂志,2004,12(5):618-620. 被引量:14
  • 2刘颖,米杰,杜军保.北京地区6~18岁儿童血脂紊乱现况调查[J].中国实用儿科杂志,2007,22(2):101-102. 被引量:32
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  • 10MOTOJIMA K, AZUMA K, KITAHARA Y,et al. Repetitive postprandial hypertriglyceridemia induces monocyte adhesion to aortie endothelial cells in Goto-Kakizaki rats. Eudocr J, 2008,55(2):373 - 379.

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