酒石酸布托啡诺预处理对小鼠心肌缺血再灌注损伤的保护作用及其机制

发布时间：2018-05-11 01:18

  本文选题：酒石酸布托啡诺 + 心肌再灌注损伤　； 参考：《东南大学学报(医学版)》2017年01期

【摘要】：目的:探讨酒石酸布托啡诺预处理对小鼠心肌缺血再灌注损伤的保护作用及其机制。方法:取雄性C57BL/6小鼠30只,随机分为3组,每组10只。缺血再灌注组(I/R组)结扎左冠状动脉前降支(LAD)30 min,再灌注6 h;布托啡诺预处理组(B+I/R组)在缺血前30 min经后肢肌肉注射酒石酸布托啡诺40μg·kg-1,余处理同I/R组;假手术组(Sham组)开胸暴露心脏,仅LAD穿线但不结扎。Sham组和I/R组小鼠在缺血前30 min肌肉注射等体积生理盐水。再灌注6 h后,采集腹主动脉血样,酶联免疫吸附法测定血清肿瘤坏死因子α(TNF-α)、肌酸激酶同工酶(CK-MB)和肌钙蛋白Ⅰ(CTnⅠ)的浓度;Western blot法测定心肌组织Cleaved caspase 8、Cleaved caspase 3、p-JNK和JNK的表达;凝胶电泳迁移率(EMSA)法测定心肌组织核因子-κB(NF-κB)结合活性。结果:与Sham组比较,I/R组血清CK-MB、CTn I和TNF-α水平显著升高(均P0.05),心肌组织Cleaved caspase 8和Cleaved caspase 3蛋白表达水平、JNK磷酸化水平以及NF-κB结合活性显著升高(均P0.05);与I/R组比较,B+I/R组血清CK-MB、CTn I和TNF-α水平显著下降(均P0.05),心肌组织Cleaved caspase 8和Cleaved caspase 3蛋白表达、JNK磷酸化水平和NF-κB结合活性显著下降(均P0.05)。结论:酒石酸布托啡诺预处理对小鼠心肌缺血再灌注损伤具有保护作用,可显著抑制I/R所致的炎症反应和心肌细胞凋亡,其机制与阻滞JNK/NF-κB信号通路相关。
[Abstract]:Aim: to investigate the protective effect and mechanism of butorphanol tartrate pretreatment on myocardial ischemia reperfusion injury in mice. Methods: thirty male C57BL/6 mice were randomly divided into 3 groups with 10 mice in each group. The left anterior descending branch of the coronary artery was ligated for 30 minutes and reperfusion for 6 hours, and butorphanol was injected intramuscularly through the hind limb 30 min before ischemia into the butorphanol 40 渭 g kg-1. The remaining treatment was the same as that in the I / R group. The heart was exposed to open chest in sham-operated group. Only mice in the LAD puncture group but not ligated. Sham group and I / R group were intramuscularly injected with normal saline 30 min before ischemia. After reperfusion for 6 h, the blood samples of abdominal aorta were collected. The concentrations of serum TNF- 伪, creatine kinase isoenzyme (CK-MBB) and troponin 鈪，

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