红景天苷对大鼠心肌缺血预处理后血管内皮生长因子表达的影响

Effect of salidroside on vascular endothelial growth factor in rats after myocardial ischemic preconditioning

目的观察红景天苷对大鼠心肌缺血/再灌注预处理后血管内皮生长因子表达的影响。方法选取16只健康大鼠,随机分为缺血/再灌注组、红景天苷预处理组,其中缺血/再灌注组、红景天苷预处理组经尾静脉注射垂体后叶素制作大鼠急性心肌缺血模型,另设8只为空白对照组。红景天苷预处理组经尾静脉注射1%红景天苷2 m L/(kg·d),每天1次,连续7 d,空白对照组和缺血/再灌注组给予等体积生理盐水预处理。于缺血预处理前及缺血预处理7 d后经眶静脉取血,采用双抗体夹心酶联免疫吸附测定(ELISA)法测定大鼠血清受体胎肝激酶1(FLK-1)及FLK-1 m RNA,缺氧诱导因子-1α(HIF-1α)及HIF-1αm RNA,心肌血管内皮生长因子(VEGF)及m RNA表达;采用测试药盒测定心肌组织中丙二醛(MDA)含量、血清超氧化物歧化酶(SOD)及过氧化氢酶(CAT)活性等指标。结果红景天苷预处理组在缺血预处理7 d后FLK-1及FLK-1 m RNA、HIF-1α及HIF-1αm RNA、VEGF蛋白质及VEGF m RNA的表达均明显增强,与空白对照组、缺血/再灌注组、预处理前比较,差异均有统计学意义(P<0.05)。同时,红景天苷预处理组CAT、SOD活性明显升高,MDA含量明显降低,与缺血/再灌注组及缺血预处理前比较,差异均有统计学意义(P<0.05)。结论红景天苷预处理急性心肌缺血大鼠,可减轻其血管内皮炎症反应及损伤程度,促使大鼠缺血心肌血管内皮新生,增强组织对自由基清除酶活性,抑制脂质过氧化反应,对急性心肌缺血再灌注损伤模型大鼠有保护作用。

Objective To observe the effect of salidroside on expression of vascular endothelial growth factor in rats after myocardial ischemic preconditioning. Methods Sixteen healthy rats were chosen and randomly divided into ischemia/reperfusion group, salidroside pretreatment group. The two groups of rats were injected Pituitrin via the tail vein to make acute myocardial ischemia model. The other 8 rats were as control group. The salidroside pretreatment group was injected 1% salidroside 2 m L/（kg·d）, once a day, for 7 days via the tail vein. The control group and ischemia/reperfusion group were given equal volume of normal saline. Blood was collected from orbital venous at two time points of before ischemic preconditioning and after ischemic preconditioning for 7 days. The expression of serum receptor FLK1 and FLK-1 m RNA, the hypoxia inducible factor-1α（HIF-1α） and HIF-1α m RNA, the myocardial VEGF and m RNA were measured by double antibody sandwich ELISA method. The malondialdehyde（MDA） content in myocardial tissues, superoxide dismutase（SOD） and catalase（CAT） activity in serum were measured by test kit. Results The expression of FLK-1 and FLK-1 m RNA, HIF-1α and HIF-1α m RNA, VEGF protein and VEGF m RNA were obviously enhanced in salidroside pretreatment group after ischemic preconditioning 7 d, the differences were statistically significant compared with control group, ischemia/reperfusion group and before ischemic preconditioning（P〈0.05）. At the same time, The CAT and SOD were significantly increased, MDA content decreased significantly in salidroside pretreatment group compared with ischemia/reperfusion group and themselves before ischemic preconditioning, the differences were statistically significant（P〈0.05）. Conclusion The salidroside pretreatment on acute myocardial ischemia reperfusion injury rats can reduce the vascular endothelial inflammation and injury degree, promote ischemic myocardial vascular endothelial rebirth, enhance the activity of the enzyme that can scavenge free radical, and inhibit lipid peroxidation, which has a protective effect on model rats with acute myocardial ischemia reperfusion injury.