血管内皮生长因子与血管重构的关系及阿托伐他汀干预作用  

Relationship between vascular endothelial growth factor and vascular remodeling in spontaneously hypertensive rats and the pharmacological mechanism of Atorvastatin

作　　者：汪俊元[1,2] 王安才[1,2] 曹蘅[1,2] 吴明[1,2] 曹晓霞[1,2] 李俊[1,2] 

机构地区：[1]皖南医学院弋矶山医院心内科,安徽芜湖241001 [2]皖南医学院心血管疾病研究所,安徽芜湖241001

出　　处：《中国现代医学杂志》2009年第9期1376-1379,1383,共5页China Journal of Modern Medicine

摘　　要：目的探讨血管内皮生长因子与血管重构的关系及阿托伐他汀干预作用。方法24只13周龄雄性自发性高血压大鼠(SHR)随机分为SHR组和阿托伐他汀组,每组12只;12只同周龄雄性WKY大鼠作为正常对照组;每组根据给药时间(4周、8周)分为两组,每组6只。4周和8周后,酶联免疫吸附法测定血浆血管内皮生长因子浓度;放射免疫法测定颈动脉血管紧张素Ⅱ浓度;病理图象管理系统测定颈动脉管腔横截面积、内弹力层围绕面积、外弹力层围绕面积,评价内膜和中膜增生程度;免疫组织化学法检测颈动脉血管内皮生长因子蛋白表达。结果与SHR组比较,阿托伐他汀组血浆血管内皮生长因子浓度明显升高,颈动脉血管内皮生长因子蛋白表达明显增强,颈动脉血管紧张素Ⅱ浓度却显著降低(P<0.01),8周末这一作用更加显著(P<0.01);SHR组内膜增生较正常对照组明显,中膜面积显著增大(P<0.01);阿托伐他汀组内膜增生和中膜面积较SHR组显著下降(P<0.01)。结论血管重构过程中,血管内皮生长因子水平下降;阿托伐他汀可逆转自发性高血压大鼠颈动脉血管重构,其机制可能是通过增加血管内皮生长因子表达而实现的。[Objective] To investigate the relationship between vascular endothelial growth factor （VEGF） and vascular remodeling in spontaneously hypertension rats （SHR）, and the intervention effect of Atorvastatin. [Methods] Thirteen-week-old male SHR （n =24） were randomized into two groups （n =12, each）： SHR group and Atorvastatin group. 12 age-matched male Wistar-Kyoto rats were selected as the normal control group （WKY group）. Each group was divided into subgroups （n =6, each） according to the duration of treatment （4 weeks, 8 weeks）. Plasma vascular endothelial growth factor （VEGF） level was measured by enzyme linked immunoserbent assay （ELISA）. Carotid artery angiotensin II （AngII） level was detected by radioimmunoassay.Lumen cross section area （LA）,Intraelastic layer area （IELA） and extraelastic layer area （EELA） were measured by computed video processing.The ratio of （IELA-LA）/（EELA-LA） was calculated. The expression of VEGF protein was determined by immunohistoehemistry method. [Results] Compared with SHR group, Plasma VEGF level and carotid artery VEGF protein expression are increased markedly in Artorvastatin group （all P 〈0.01）, while carotid artery AngII level is reduced signifieandy （P 〈 0.01）, these effects are further strengthened at the end of eight weeks （all P 〈0.01）. The hyperplasia of intima in SHR group is more significantly exacerbated than that in normal control group （P 〈0.01）, which is markedly inhibited in Artorvastatin group （P 〈0.01）. [Conclusions] VEGF level is decreased in the progression of vascular remodeling. Vascular remodeling in carotid artery is markedly reversed by Artorvastatin in SHR, which may be related to the increased expression of VEGF protein.

关 键 词：自发性高血压大鼠 血管内皮生长因子 血管重构 阿托伐他汀 

分 类 号：R972[医药卫生—药品]