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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 observe the effect of IPost on serum cytokines in rats after myocardial ischemia, and to explore the role of endothelial nitric oxide synthase and its mechanism. Methods: Fifty SD male rats were randomly divided into 5 groups: sham operation group (A group), ischemia / reperfusion group (B group), IPost group (C group), L- L.NAME + I / R group (group D) and L.NAME + IPost group (group E). The model of I / R injury was established by ligation of left anterior descending coronary artery. Except for group A, the other groups were given ischemia for 30 min and reperfused for 2 h. C and E groups were given 3 cycles immediately after ischemia for 30 min Of 10 s reperfusion and 10 s ischemia; group D and E were given L.NAME before ischemia. Blood samples were collected at 15 min, 30 min, 1 h, and 2 h after reperfusion to determine the levels of interleukin (IL) -6 and IL-10; 2 h after reperfusion, the rats were sacrificed and the area of infarction percentage. Results: ① The percentage of myocardial infarction area in transverse plane in group C was less than that in group B (P <0.05), that in group E was greater than that in group C (P <0.05), but there was no significant difference between group D and group B (P> 0.05) .②Compared with group B, the level of IL-6 in group C was lower and the level of IL-10 was higher; ③ Compared with group C, the level of IL-6 in group E was increased and the level of IL-10 was decreased; There was no significant difference in the levels of IL-6 and IL-10 between the two groups. CONCLUSION: IPost can reduce the level of pro-inflammatory cytokines (IL-6) and anti-inflammatory cytokines (IL-10), which may be related to the involvement of endothelial nitric oxide synthase in the regulation of inflammatory cytokines.