本文選題：羥可酮　切入點：后處理　出處：《蘭州大學》2017年碩士論文　論文類型：學位論文

【摘要】：目的:探討羥考酮后處理對大鼠心肌缺血再灌注損傷的影響。方法:成年健康雄性SD大鼠50只,體重200~300 g,采用隨機數(shù)字表法分為5組(n=10):假手術組(S組)、缺血再灌注組(I組)、羥考酮后處理組(O組)、κ受體阻斷劑nor-binaltorphimine(Nor-BNI)組(N組)和PKC選擇性抑制劑白屈菜紅堿(chelerythrine)組(CH組)。采用結扎冠狀動脈前降支30min、開放120min的方法建立心肌缺血再灌注模型。S組只穿線,不結扎左冠狀動脈前降支;N組與CH組分別于造模前給予Nor-BNI 2mg/kg和白屈菜紅堿5mg/kg,給予后立即結扎;O組、N組與CH組于再灌注前2min經(jīng)頸靜脈注入羥考酮0.5mg/kg。于再灌注120 min時采集動脈血樣,測定血清心肌肌鈣蛋白I(cTnI)和肌酸激酶同工酶(CK-MB)的濃度。快速處死大鼠后,取心臟,檢測心肌梗死程度(TTC染色法)。結果:與S組比較,I組、O組、N組和CH組血清cTnI和CK-MB的濃度升高,心肌梗死體積明顯增大(P0.05);與I組比較,O組、N組和CH組血清cTnI和CK-MB的濃度降低,心肌梗死體積減小(P0.05);與O組比較,N組和CH組血清cTnl和CK-MB的濃度升高,心肌梗死體積增大(P0.05)。結論:羥考酮后處理可減輕大鼠心肌缺血再灌注損傷,其作用機制可能與激活κ受體,進而激活PKC通道有關。
[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.
【學位授予單位】：蘭州大學
【學位級別】：碩士
【學位授予年份】：2017
【分類號】：R614

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