论文部分内容阅读
目的:探讨法舒地尔对急性心肌梗死(AMI)大鼠炎性细胞因子表达的影响及细胞因子表达与Rho激酶的关系。方法:选取雄性Wistar大鼠,建立大鼠AMI模型,将术后存活大鼠随机分为治疗组(F组)和AMI组;另设假手术组(S组),只在其左前降支下穿线不结扎。F组给予法舒地尔5mg/kg,AMI组和S组给予等量0.9%氯化钠溶液,腹腔注射,每日2次。4周后,用Nikon 4多导生理记录仪检测血流动力学指标,放射免疫法测血清中肿瘤坏死因子(TNF)-α和白细胞介素-1β(IL-1β)含量,EvensBlue及NBT双染确定缺血及梗死面积,RT-PCR法测定Rho激酶mRNA的表达。结果:与S组相比,AMI组细胞因子TNF-α和IL-1β、左室舒张末压(LV-EDP)表达明显升高,而左室收缩压(LVSP)和左室压力上升/下降最大速率(±dp/dtmax)明显减低(P<0.05)。与AMI组比较,F组梗死面积显著减小,TNF-α和IL-1β表达水平明显下降,Rho激酶mRNA表达显著减少;F组更明显地降低LVEDP,升高LVSP和±dp/dtmax(P<0.01),左室功能明显改善。结论:法舒地尔可以降低AMI大鼠炎性细胞因子及心肌Rho激酶表达,保护缺血心肌,减少心肌梗死面积,改善心功能。
Objective: To investigate the effect of fasudil on the expression of inflammatory cytokines in acute myocardial infarction (AMI) rats and the relationship between cytokines and Rho kinase. Methods: Male Wistar rats were selected to establish rat AMI model. The survived rats were randomly divided into treatment group (F group) and AMI group. Another sham operation group (S group) was established only in the left anterior descending branch Threading is not ligation. F group was fasudil5mg / kg, AMI group and S group were given the same amount of 0.9% sodium chloride solution, intraperitoneal injection twice a day. After 4 weeks, the hemodynamic parameters were measured with a Nikon 4 multi-channel physiologic recorder. The levels of TNF-α and IL-1β in the serum were measured by radioimmunoassay. The contents of EvensBlue and NBT To determine the area of ischemia and infarction, Rho kinase mRNA expression was determined by RT-PCR. Results: Compared with S group, the expression of TNF-α, IL-1β and LV-EDP in AMI group were significantly increased, while LVSP and LVP increased / decreased The maximum rate (± dp / dtmax) was significantly reduced (P <0.05). Compared with AMI group, the infarct size in F group was significantly reduced, the expression of TNF-α and IL-1β was significantly decreased and Rho kinase mRNA expression was significantly decreased in F group; LVEDP, LVSP and ± dp / dtmax (P <0.01), left ventricular function improved significantly. Conclusion: fasudil can reduce the expression of inflammatory cytokines and Rho kinase in AMI rats, protect the ischemic myocardium, reduce the area of myocardial infarction and improve cardiac function.