血管内皮生长因子与细胞黏附分子-1的表达及其对血管内皮功能的影响  

Expressions of vascular endothelial growth factor and vascular cell adhesion molecule-1 in hyperlipidemic rats and their impact on endothelial function

作　　者：吴峻[1] 孙明[2] 周宏研[2] 林锦潮[1] 何兆初[1] 区碧如[1] 

机构地区：[1]广州医学院第一附属医院心内科,510120 [2]中南大学湘雅医院心内科

出　　处：《中华老年医学杂志》2007年第9期689-692,共4页Chinese Journal of Geriatrics

基　　金：广东省自然科学基金资助项目（5300999）

摘　　要：目的通过观察高脂血症大鼠NO、血管内皮生长因子（VEGF）与血管细胞黏附分子-1 （VCAM-1）水平及调脂药物辛伐他汀对其表达的影响,探讨高脂血症在动脉粥样硬化早期对内皮功能的损伤机制。方法将30只SD大鼠随机分为正常对照组、高脂血症组及辛伐他汀治疗组,分别检测3组大鼠血脂变化及NO、VEGF、VCAM-1水平。结果与正常对照组比较,高脂血症组NO水平较低、VCAM-1表达较强且范围较广,黏附于内皮的白细胞数明显增多（P〈0.05）;VEGF水平与对照组比较,差异无统计学意义;高脂血症组血NO2^-/NO3^-水平为（29.6±7.2）μmol/L,与正常对照组（38.0±9.9）μmol/L比较明显降低（P〈0.05）;辛伐他汀组血NO2^-/NO3^-水平为（37.4±9.5）μmol/L,高于高脂血症组（P〈0.05）,VEGF较高脂血症组明显增高（P〈0.05）;血NO2^-/NO3^-与VEGF呈正相关（r=0.644,P〈0.05）。血清NO浓度与VCAM-1表达强度及范围呈负相关（r分别为-0.676、-0.684,均为P〈0.05）。结论NO、VCAM-1参与高脂血症血管内皮的损害;辛伐他汀对内皮功能的改善,可能是通过提高NO水平、减少内皮细胞VCAM-1的表达及促进VEGF的分泌而实现的。Objective To observe the serum levels of vascular endothelial growth factor（VEGF） and vascular cell adhesion molecule-1（VCAM-1）,and explore the impact of hyperlipidemia on endothelial function during the early stage of atherosclerosis.Methods Thirty Sprague-Dawley rats were randomly divided into 3 groups：control group,hyperlipidemic group and simvastatin treated group.Serum levels of total cholesterol（TC）,triglyceride（TG）and NO,VEGF,VCAM-1 were measured.Results Compared with the control,hyperlipidemic rats had lower level of NO,stronger and more widely expressed VCAM-1.Moreover,there was an increase in leukocyte accumulation on the endothelial surface.NO2^-/NO3^- level in hyperlipidemic group[（29.6±7.2）μmol/L]was lower than control group[（38.0±9.9）μmol/L]（P〈0.05） ,and simvastatin treated group[（37.4±9.5）μmol/L] （P〈0.05）.VEGF level in simvastatin treated group was higher than in hyperlipidemic group（P〈0.05）.Serum NO2^-/NO3^- level was possitive correlated with VEGF level（r=0.644,P〈0.05）,and negative correlated with VCAM-1 expression（r=-0.676、-0.684,all P〈0.05）.Conclusions The NO activity could be inhibited by hyperlipidemia which facilitates the endothelial impairment of VCAM-1.Simvastatin could restore endothelial function probably by increasing NO and VEGF levels, decreasing VCAM-1 level.

关 键 词：高脂血症 一氧化氮 NO 血管内皮生长因子类 血管细胞黏附分子-1 

分 类 号：R686[医药卫生—骨科学]