摘要
目的:观察大鼠心肌缺血后适应(IPost)对血清细胞因子的影响,探讨内皮型一氧化氮合酶的作用及其机制。方法:50只SD雄性大鼠随机分为5组:假手术组(A组)、缺血再灌注(I/R)组(B组)、IPost组(C组)、左旋硝基精氨苯甲酯(L.NAME)+I/R组(D组)和L.NAME+IPost组(E组)。结扎冠状动脉左前降支建立I/R损伤模型,除A组外,其余各组均行缺血30 min、再灌注2 h;C组和E组分别在缺血30 min后立即给予3个循环的10 s再灌注和10 s缺血;D组和E组在缺血前再给予L.NAME。再灌注15 min、30 min、1 h、2 h时取血,测定白细胞介素(IL)-6和IL-10水平;再灌注2 h取血后处死大鼠,计算梗死面积占横切面的百分比。结果:①C组大鼠心肌梗死面积占横切面的百分比小于B组(P<0.05),E组大于C组(P<0.05),而D组与B组之间差异无统计学意义(P>0.05);②与B组比较,C组IL-6水平较低,IL-10水平较高;③与C组比较,E组IL-6水平升高,IL-10水平降低;④B组与D组IL-6和IL-10水平比较差异均无统计学意义。结论:IPost能降低促炎细胞因子(IL-6)、升高抗炎细胞因子(IL-10)水平,其机制可能与内皮型一氧化氮合酶参与炎症因子的调节有关。
Objective:To determine whether ischemic postconditioning(IPost)could affect the level of inflammatory cytokines and the role of endothelial nitric oxide synthase in this phenomenon.Method:Male SD rats(n=50) were randomly divided into five groups,including sham group,ischaemia/reperfusion(I/R) group,IPost group,L.NAME-treated before postconditiong(L.NAME+IPost) group and L.NAME-treated before I/R(L.NAME+I/R) group.In this process,blood was drawn to assay serum IL-6 and IL-10 levels at 15 min,half an hour,one hour and two hour after reperfusion.Rats were killed for measuring myocardial infarct size.Result:IPost reduced the infarct size(P0.05),and this protection disappeared when L.NAME was given before I/R.IPost could reduce the serum level of IL-6 and increase the level of IL-10 in the IPost group compared with those in the I/R group(P0.05),but such changes had not shown when L.NAME was given beforeI/R.There was no significant difference of IL-10 and IL-6 levels between the I/R group and L.NAME+I/R group(P0.05).Conclusion:The protective effect of ischemic postconditioning may be retated to decrease of proinflammatory cytokine level and increase of anti-inflammatory cytokine level which are modulated by enhancement of endothelial nitric oxide synthase activity.
出处
《临床心血管病杂志》
CAS
CSCD
北大核心
2011年第5期389-392,共4页
Journal of Clinical Cardiology
基金
国家自然科学基金资助项目(No:30871008)