摘要
目的 :评价辛伐他汀是否促进缺血心肌毛细血管新生。方法 :雄性Wistar大鼠 30只 ,成功复制心肌梗死模型 2 4h后随机分成辛伐他汀组、对照组和辛伐他汀 +N 硝酸 l 精氨酸甲酯 (l NAME)组 ,分别ip辛伐他汀 2mg·kg- 1·d- 1、生理盐水和辛伐他汀 2mg·kg- 1·d- 1+l -NAME15mg·kg- 1·d- 1。 4wk后应用免疫组化法及化学法检测各组大鼠缺血心肌中血管内皮细胞生长因子 (VEGF)蛋白质表达、一氧化氮 (NO )水平及毛细血管密度。结果 :与对照组相比辛伐他汀组大鼠缺血心肌中毛细血管密度显著增加 (196 3±s 10 8)·mm- 2 (P <0 .0 1) ,NO水平明显增高 (2 6± 5 )mmol·kg- 1(P <0 .0 1) ,但VEGF表达无明显改变 ;加用l NAME后 ,辛伐他汀的这些作用消失。结论 :辛伐他汀可促进大鼠缺血心肌毛细血管新生 ,NO可能介导了此作用。
AIM: To evaluate whether simvastatin can promote angiogenesis of ischemic myocardium. METHODS: Thirty male rats after 24 h of successful establishment of myocardial infarction model were randomly divided into simvastatin group(simvastatin 2 mg·kg -1·d -1, ip), control group(normal saline, ip) and simvastatin plus N-nitrol-arginine methyl ester (l-NAME,inhibitor of nitric oxide synthase) group(simvastatin 2 mg·kg -1·d -1+l-NAME 15 mg·kg -1·d -1, ip). The capillary density, expression of vascular endothelial growth factor(VEGF) protein and level of nitric oxide (NO) of all groups were detected by immunohisto-chemistry and chemistry methods at 4 wk after the treatment. RESULTS: Capillary density (1 963±s 108)·mm -2 and level of NO (26±5) mmol·kg -1 in ischemic myocardium significantly augmented at simvastatin group compared with that at control group(P< 0.01), but expression of VEGF protein was in the absence of changes between the two groups. After simvastatin plus l-NAME treatment, level of NO in ischemic myocardium significantly decreased, and the effect of simvastatin on the promotion of new blood vessel growth disappeared. CONCLUSION: Simvastatin can promote angiogenesis of ischemic myocardium in rats. NO may play a role in angiogenesis.
出处
《中国新药与临床杂志》
CAS
CSCD
北大核心
2004年第6期328-331,共4页
Chinese Journal of New Drugs and Clinical Remedies
关键词
心肌梗死
动物
实验
辛伐他汀
毛细血
管新生
myocardial infarction
animals, laboratory
simvastatin
angiogenesis
