CAJ | 학술논문

目的：探讨20‐羟二十烷花生四烯酸（20‐HETE）在离体心肌缺血再灌注损伤中的影响及机制。方法大鼠离体心脏通过Langendorff装置建立缺血再灌注模型，心脏缺血35 min再灌注40 min。缺血前10 min开始分别灌流HET0016（1μmol／L）及不同浓度的20‐HETE（10、30、50 nmol／L），直至整个缺血再灌注结束。通过Powerlab／8P系统实时记录离体心脏血流动力学指标；心肌梗死面积采用TTC染色法测定；活性氧簇（ROS）及蛋白质羰基化水平分别使用DHE荧光探针法和DNPH法检测。结果灌流液中使用 HET0016显著改善了缺血诱导的心肌收缩力的下降，抑制20‐HETE的生成后，减少了心肌梗死面积的发生（P＜0．05）；而灌流液中外源性加入20‐HETE后加重了心肌再灌注后损伤（P＜0．05）。同时，HET0016明显降低了再灌注后ROS的生成及蛋白质过氧化，而加入20‐HETE后显著促进了ROS生成和蛋白质过氧化（P＜0．05）。结论20‐HETE通过增加ROS生成导致蛋白质过氧化加重心肌缺血再灌注损伤。
목적：탐토20‐간이십완화생사희산（20‐HETE）재리체심기결혈재관주손상중적영향급궤제。방법대서리체심장통과Langendorff장치건립결혈재관주모형，심장결혈35 min재관주40 min。결혈전10 min개시분별관류HET0016（1μmol／L）급불동농도적20‐HETE（10、30、50 nmol／L），직지정개결혈재관주결속。통과Powerlab／8P계통실시기록리체심장혈류동역학지표；심기경사면적채용TTC염색법측정；활성양족（ROS）급단백질탄기화수평분별사용DHE형광탐침법화DNPH법검측。결과관류액중사용 HET0016현저개선료결혈유도적심기수축력적하강，억제20‐HETE적생성후，감소료심기경사면적적발생（P＜0．05）；이관류액중외원성가입20‐HETE후가중료심기재관주후손상（P＜0．05）。동시，HET0016명현강저료재관주후ROS적생성급단백질과양화，이가입20‐HETE후현저촉진료ROS생성화단백질과양화（P＜0．05）。결론20‐HETE통과증가ROS생성도치단백질과양화가중심기결혈재관주손상。
Objective To investigate the effect of 20‐HETE on the isolated myocardial ischemia reperfusion injury and to ex‐plore its underlying mechanisms .Methods Experiments were performed in isolated rat hearts subjected to 35 min of ischemia fol‐lowed by 40 min of reperfusion in Langendorff preparations .HET0016 (1 μmol/L) and various concentrations (10 ,30 or 50 nmol/L) of 20‐HETE were infused 10 min before the onset of ischemia and throughout the reperfusion period .Cardiac hemodynamic changes and myocardial contractility were continuously recorded with the Powerlab /8P system .Myocardial infarct size was meas‐ured by TTC staining .The level of ROS and the protein carbonyl content were determined by DHE fuorescence and DNPH method , respectively .Results Perfusion with HET0016 significantly improved myocardial ischemia reperfusion injury reduction in cardiac contractility ,after inhibited the production of 20‐HETE significantly reduced the occurrence of myocardial infarction area (P<0 .05) ,but exogenous join 20‐HETE aggravated I/R‐induced myocardial injury (P<0 .05) .Myocardial ischemia reperfusion injury significantly increased production of ROS and oxidative stress ,both of which were significantly inhibited by HET 0016 and enhanced by 20‐HETE administration(P< 0 .05) .Conclusion 20‐HETE stimulates ROS production and enhance protein carbonylation , which aggravates myocardial ischemia reperfusion injury .