羟考酮后处理对大鼠心肌缺血再灌注损伤的影响

发布时间：2018-03-03 07:22

本文选题：羟可酮　切入点：后处理　出处：《兰州大学》2017年硕士论文　论文类型：学位论文

【摘要】：目的:探讨羟考酮后处理对大鼠心肌缺血再灌注损伤的影响。方法:成年健康雄性SD大鼠50只,体重200~300 g,采用随机数字表法分为5组(n=10):假手术组(S组)、缺血再灌注组(I组)、羟考酮后处理组(O组)、κ受体阻断剂nor-binaltorphimine(Nor-BNI)组(N组)和PKC选择性抑制剂白屈菜红碱(chelerythrine)组(CH组)。采用结扎冠状动脉前降支30min、开放120min的方法建立心肌缺血再灌注模型。S组只穿线,不结扎左冠状动脉前降支;N组与CH组分别于造模前给予Nor-BNI 2mg/kg和白屈菜红碱5mg/kg,给予后立即结扎;O组、N组与CH组于再灌注前2min经颈静脉注入羟考酮0.5mg/kg。于再灌注120 min时采集动脉血样,测定血清心肌肌钙蛋白I(cTnI)和肌酸激酶同工酶(CK-MB)的浓度。快速处死大鼠后,取心脏,检测心肌梗死程度(TTC染色法)。结果:与S组比较,I组、O组、N组和CH组血清cTnI和CK-MB的浓度升高,心肌梗死体积明显增大(P0.05);与I组比较,O组、N组和CH组血清cTnI和CK-MB的浓度降低,心肌梗死体积减小(P0.05);与O组比较,N组和CH组血清cTnl和CK-MB的浓度升高,心肌梗死体积增大(P0.05)。结论:羟考酮后处理可减轻大鼠心肌缺血再灌注损伤,其作用机制可能与激活κ受体,进而激活PKC通道有关。
[Abstract]:Objective: to investigate the effect of hydroxycodone post-treatment on myocardial ischemia-reperfusion injury in rats. Weighing 200g / 300g, the rats were randomly divided into 5 groups: sham operation group (group S), ischemia-reperfusion group (group I), hydroxycodone group (group O), 魏 receptor blocker nor-binaltorphimine (Nor-BNIN) group (n) and PKC selective inhibitor, chelerythrine (group Ch). To establish myocardial ischemia-reperfusion model by ligating anterior descending coronary artery for 30 min and opening it for 120 min. The left anterior descending branch of coronary artery was not ligated in group N and group Ch were given Nor-BNI 2 mg / kg and chrythrine 5 mg / kg before modeling, respectively. Immediately after administration, the N group and Ch group were immediately ligated with hydroxone 0.5 mg / kg via jugular vein before reperfusion. Arterial blood samples were collected at 120 min after reperfusion. The serum levels of cardiac troponin I (cTnI) and creatine kinase isoenzyme (CK-MBB) were measured. After the rats were killed quickly, the myocardial infarction degree was detected by TTC staining. Results: compared with the S group, the serum cTnI and CK-MB levels in the N group and Ch group were higher than those in the S group. Compared with group I, the concentration of serum cTnI and CK-MB decreased, and the volume of myocardial infarction decreased (P 0.05), and the concentrations of serum cTnl and CK-MB increased in group N and Ch. Conclusion: hydroxycodone post-treatment can reduce myocardial ischemia-reperfusion injury in rats, and its mechanism may be related to activation of 魏 receptor and activation of PKC channel.
【学位授予单位】：兰州大学
【学位级别】：硕士
【学位授予年份】：2017
【分类号】：R614

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