氟伐他汀对兔心肌梗死再灌注血清白细胞介素-8及梗死面积的影响

Effects of pretreatment with fluvastatin on serum interleukin-8 and areas of myocardial infarction in reperfusion injury rabbits after myocardial infarction

目的:观察氟伐他汀预处理对血清白细胞介素8(IL8)及心肌梗死面积的影响,探讨其对心肌梗死再灌注损伤保护作用的可能机制。方法:健康新西兰白兔24只,随机分为3组:假手术组、对照组、氟伐他汀组(氟伐他汀10mg·kg-1·d-1),每组8只。除假手术组外,其余2组通过结扎冠状动脉前降支60min,然后松开180min建立心肌梗死再灌注动物模型。在实验终点采右心房血,分离血清,检查IL8、CKMB含量,处死动物取出心脏,用1%氯化三苯基四氮唑染色后计算梗死心肌面积,并检测梗死区心肌髓过氧化酶(MPO)含量。结果:对照组、氟伐他汀组IL8、MPO活性明显高于假手术组(均P<0.05),氟伐他汀组IL8、MPO活性低于对照组(均P<0.05)。对照组血清CKMB明显高于假手术组(P<0.01),氟伐他汀组CKMB也明显高于假手术组(P<0.05),但较对照组明显降低(P<0.05)。氟伐他汀组心肌梗死面积[(26.90±1.81)%]较对照组[(31.22±2.31)%]小(P<0.05)。结论:氟伐他汀能通过抑制IL8的合成,减少中性粒细胞的浸润,从而改善心肌缺血再灌注损伤。

Objective：To investigate the effects of the pretreatment with fluvastatin on serum interleukin-8 and areas of myocardial infarction （MI） in reperfusion injury rabbits after MI. Method：Twenty-four male New Zealand white rabbits were randomly divided into three groups： sham group（ n = 8）, control group（ n = 8） and fluvastatin group（ n =8）. Both of the former 2 groups were fed daily with ordinary food while the animals of fluvastatin group pretreated with fluvastatin 10 mg · kg^-1 · d^-1. Models of ischemia/reperfusion were established in both control and fluvastatin groups by a sixty-minute coronary occlusion followed by a three-hour reperfusion. Blood samples were extracted from the right atrium of the animals, and the sera were collected with hypothermia high speed centrifugation for the measurement of IL-8 and creatine kinase-MB （CK-MB）. MI size was determined by triphenyltetrazolium chloride staining, and the cardiac muscle in MI was frozed for detecting myeloperoxidase （MPO）. Result.. In control and fluvastatin groups, the levels of serum IL-8 , MPO, and CK-MB were all elevated significantly compaired with those in sham group,especially those in control group, P 〈0. 05. further more, MI sizes of animals in Fluvastatin were markedly smaller than those in control group （[26.90± 1. 81]% vs [31.22± 2. 33]%, P〈0. 05）. Concision： Fluvastatin could improve myocardial ischemia/reperfusion injury by inhibiting the product of IL-8 and reducing inflammatory cell infiltration.