寒潮诱发高血压大鼠卒中发病前CD62p和细胞间黏附分子1的变化
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湖南省教育厅科学研究项目(06c708)


Changes of CD62p and Intercellular Adhesion Molecule-1 in Rats with Pro-Stroke Status Caused by Artificial Cold
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    摘要:

    目的研究血小板活化和血管内皮损伤标志物在脑卒中启动中的作用。方法300只SD大鼠分为模型组、假手术组和正常对照组,其中假手术组再分为假手术和假手术+内皮损伤组;模型组再分为高血压组、内皮损伤组和高血压+内皮损伤组;在第12周时使用寒潮箱处理各组大鼠,将各组大鼠再分为寒潮组和非寒潮组,其中寒潮组分别在寒潮前及寒潮后检测CD62p阳性表达率,免疫组织化学检测脑小血管细胞间黏附分子1的表达。结果模型组大鼠CD62p阳性表达率和细胞间黏附分子1的表达量高于正常对照组和假手术组(P<0.05);模型组大鼠经寒潮处理后CD62p阳性表达率和细胞间黏附分子1的表达量明显高于非寒潮组(P<0.05),其中高血压+内皮损伤组CD62p阳性表达率和细胞间黏附分子1的表达量更高(P<0.05)。结论长期的高血压损害了大鼠的内皮系统,而寒潮可以使这种损害加重,使其接近卒中前状态。

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    AimTo investigate the contribution of platelet activation and the damage marker of blood vessel endothelium in stroke.Methods300 SD rats were divided into three groups: model group, sham operated group and normal control group, the sham operated group were divided into sham operated group and sham operated+endothelium damage group; the model group were divided into hypertension group, endothelium damage group and hypertension+endothelium damage group.In the 12th week the rats were divided into artificial cold exposure (ACE) and non-ACE, only ACE were endured by artificial climate cabinet, blood samples were collected for measuring CD62p expression and brain tissues were got to analyse intercellular adhesion molecule-1 (ICAM-1) expression.ResultsIn model group, the CD62p and ICAM-1 expression were higher than other groups (P<0.05); the CD62p and ICAM-1 expression in ACE (model group) were higher than non-ACE group (P<0.05); the CD62p and ICAM-1 expression in hypertension+endothelium damage group was the highest in model group (P<0.05).ConclusionPersistent hypertension could damage the endothelium system of rat, artificial cold would worse this damage, and make it close to the state of pro-stroke.

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夏鹏飞,高帆,聂亚雄.寒潮诱发高血压大鼠卒中发病前CD62p和细胞间黏附分子1的变化[J].中国动脉硬化杂志,2010,18(2):114~116.

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  • 收稿日期:2009-11-23
  • 最后修改日期:2010-02-05
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