摘要
目的:建立大鼠实验性心肌缺血再灌注损伤动物模型,观察丹红注射液对其血管内皮生长因子(vascular endothelial growthfactor,VEGF)表达的影响及氧化应激的作用,探讨其作用机制。方法:40只大鼠随机分为实验性心肌缺血组(IR)、血管内皮生长因子B组(VEGFB)、丹红小剂量(DS1)、大剂量组(DS2),经尾静脉注射垂体后叶素造成大鼠实验性心肌缺血再灌注损伤动物模型,另设8只空白对照组(BCG),均采用尾静脉注射液给药治疗,并于治疗前、7 d、14 d后3个时点分别检测VEGF蛋白质及Mrna、FLK-1、FLK-1 m RNA的表达,心肌丙二醛(MDA)、肌酸激酶同工酶(CK-MB)等指标,借此考察丹红注射液对大鼠实验性心肌缺血再灌注损伤VEGF表达的影响。结果:丹红注射液明显增强DS1、DS2组VEGF蛋白质及m RNA、FLK-1的阳性表达,增加CK-MB活性,降低MDA的合成,与IR比较(P<0.05),差异均有统计学意义,DS1、DS2组各指标比较,P>0.05,差异无统计学意义。结论:丹红注射液有与VEGFB类似的减轻大鼠实验性心肌血管内皮炎症反应,促进血管内皮细胞增殖、诱导缺血部位血管新生及改善血管内皮功能紊乱的作用,其作用机制可能与其促进VEGF的分泌,抑制心肌缺血时脂质过氧化,促进氧自由基清除酶清除氧自由基有关,对大鼠实验性心肌缺血再灌注损伤有保护作用。
Objective：To establish a rat model of experimental myocardial ischemia reperfusion injury animal model,effects of Danhong Injection on the vascular endothelial growth factor（vascular,endothelial growthfactor,VEGF）affects the expression and role of oxidative stress,and to explore its mechanism of action. Methods：40 rats were randomly divided into experimental myocardial ischemia group（IR）,small dose group（DS1）,Dan red（DS2）,via the tail vein injection of pituitrin caused animal model in rats with experimental myocardial ischemia reperfusion injury,another 8 only blank control group（BCG）,adopt the tail vein injection to drugs,and before treatment,7 d,14 d after three point was used to detect the VEGF protein expression and Mrna,FLK-1,FLK-1m RNA,myocardial malondialdehyde（MDA）,creatine kinase isoenzyme MB（CK-MB）and other indicators,the investigation of Danhong Injection on experimental myocardial ischemia in rats effects of reperfusion injury VEGF expression. Results：Danhong Injection significantly enhanced the positive expression of DS1,VEGF protein and m RNA in group DS2,FLK-1,increase CK-MB activity,decrease the synthesis of MDA,compared with IR（P〈0.05）,the difference was statistically significant,DS1,DS2 group of each index comparison,P〈0.05,the difference was not statistically significant. Conclusion：Danhong Injection and VEGF-B to reduce the experimental rat myocardial vascular endothelial inflammation,promote the proliferation of vascular endothelial cells induced by ischemia,angiogenesis and improve the site of vascular endothelial dysfunction,and its mechanism may be related to the promotion of VEGF secretary,lipid peroxidation inhibition of myocardial ischemia,promote oxygen free radical scavenging enzymes scavenging oxygen free radicals,on experimental myocardial ischemia reperfusion injury in rats has a protective effect.
出处
《辽宁中医药大学学报》
CAS
2015年第12期35-38,共4页
Journal of Liaoning University of Traditional Chinese Medicine
