C-反应蛋白基因过表达诱导SD大鼠血压升高的实验研究

Effects of Eukaryotic Expression Vector pcDNA3.1 Mediated C-Reactive Protein Gene on Blood Pressure in Sprague-Dawley Rats

目的研究C-反应蛋白(C-reactive protein,CRP)重组质粒过表达诱导SD大鼠发生高血压,继而引起心血管功能障碍和重塑。方法18只SD大鼠随机分为3组,每组6只,分别给予尾静脉注射pcD-NA3·1-CRP重组质粒、pcDNA3·1空质粒及生理盐水。定期检测尾动脉血压,28d后处死动物,并于处死动物前进行心脏血流动力学、血管张力及心血管系统重塑分析。结果实现C-反应蛋白在大鼠体内的过表达。与两个对照组相比较,pcDNA3·1-CRP组血压升高的同时,伴有心脏收缩与舒张功能的显著障碍,胸主动脉舒张功能显著降低,心血管系统重塑。结论炎性因子C-反应蛋白可以引起血压升高。

Objective To explore the effects of overexpression of C-reactive protein on blood pressure and cardiovascular dysfunction and remodeling in Sprague-Dawley rats. Methods Eighteen Sprague-Dawley rats were randomly divided into three groups. The rats were intravenously injected PcDNA3.1 mediated C-reactive protein gene, pcDNA3.1 or 0. 9% sodium respectively. Twentyeight days after the injection, cardiac haemodynamics of all rats were measured and vascular tone and cardiovascular remodeling were examined. Results C-reactive protein expression was observed in vivo. Compared with controls, increased blood pressure, decreased cardiac systolic and diastolic function, reduced diastolic function of thoracic aorta, and cardiac remodeling were noted in the group of pcDNA3.1 mediated C-reactive protein gene. Conclusions C-reactive protein as an inflammatory factor may be associated with hypertension.