王建礼,徐兴华,张华.辛伐他汀对兔慢性缺血心肌血管新生及VEGF表达的影响[J].济宁医学院学报,2013,(4):250-252 |
辛伐他汀对兔慢性缺血心肌血管新生及VEGF表达的影响 |
The influence of simvastatin on angiogenesis and the expression of VEGF induced by chronic ischemic mycardium in rabbits |
投稿时间:2013-05-25 |
DOI:10.3969/j.issn.1000-9760.2013.04.005 |
中文关键词: 心肌缺血;血管新生;辛伐他汀;血管内皮生长因子 |
英文关键词: Myocardial ischemia, Angiogenesis, Simvastatin, Vascular endothelial growth factor |
基金项目:济宁医学院2008年青年科学基金项目 |
作者 | 单位 | 王建礼 | 济宁医学院基础学院, 山东济宁 272067 中国国土资源航空物探遥感中心门诊部, 北京 100083 | 徐兴华 | 济宁医学院基础学院, 山东济宁 272067 中国国土资源航空物探遥感中心门诊部, 北京 100083 | 张华 | 济宁医学院基础学院, 山东济宁 272067 中国国土资源航空物探遥感中心门诊部, 北京 100083 |
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中文摘要: |
目的 研究辛伐他汀对慢性缺血心肌血管新生的促进作用。方法雄性新西兰大白兔36只,随机化分为3组:对照组、模型组、辛伐他汀治疗组。对照组仅进行开胸手术;模型组在左冠状动脉回旋支上放置Ameroid缩窄环,复制慢性心肌缺血模型;辛伐他汀治疗组为左冠状动脉回旋支上放置Ameroid缩窄环后,每日1次给予辛伐他汀灌胃,用量为3 mg/kg,共21d。以Ⅷ因子相关抗原的抗体进行免疫组化染色,计数毛细血管数目及毛细血管密度(毛细血管数/mm2)。免疫组化法测定缺血心肌中VEGF的表达。结果辛伐他汀治疗组毛细血管密度显著高于模型组;辛伐他汀治疗组慢性缺血心肌中VEGF的表达量显著高于模型组。结论 辛伐他汀可促进慢性缺血心肌中血管的新生,其机制可能与其增加慢性缺血心肌中VEGF的表达相关。 |
英文摘要: |
Objective To study the influence of simvastatin on angiogenesis in chronic ischemic mycardium.Methods 36 male New Zealand albino rabbit were randomized into 3 groups:control group, model group and simvastatin treatment group.The animals in control group received thoracotomy only;the animals in model group were placed an Ameroid constrictor on left circumflex coronary artery, thus leading to chronic mycardial ischemia;the animals in simvastatin treatment group were placed an Ameroid constrictor on left circumflex coronary artery, followed by lavaged with simvastatin at 3 mg/kg once daily for 21 days.Immunohistochemisty stain was performed with antibody of factorⅧrelated antigen to determine the capillary density(number of capillary/mm2).Immunohistochemisty staining was performed to determine the expression of VEGF in ischemic mycardium.Results The capillary density in Simvastatin treatment group was higher than model group;the expression of VEGF in chronic ischemiac mycardium in Simvastatin treatment group was higher than model group.Conclusion Simvastatin treatment can promote angiogenesis in chronic ischemic mycardium, and its mechanism is likely to be associated with the increase of VEGF expression in chronic ischemic mycardium. |
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