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目的建立大鼠离体心脏心肌缺血再灌注模型,初步探讨咖啡酸苯乙酯对离体心脏心肌缺血再灌注损伤的保护作用。方法雄性SD大鼠30只,取心脏Langendorff法离体灌流,实验分5组:空白组:KH(Krebs-Henseleit)液连续灌流100 min;模型组:KH液稳灌30 min后停灌30 min,再灌注KH液40 min;给药组:KH液稳灌30 min后,停灌30 min,再灌注3、6和12 mg/L CAPE的KH液40min。实验中观察各组大鼠离体心脏的冠脉流量、心肌收缩力及心率的变化。停灌后测其各组心肌组织的丙二醛(MDA)、蛋白羰基化(PCO)的含量和超氧化物歧化酶(SOD)活性。结果心脏缺血再灌注期间,模型组收缩力减弱,张力增加,心率减慢,冠脉流量明显减少,出现心律失常;给药组在再灌注后收缩力增强,张力降低,心率增快,冠脉流量明显增加,节律整齐。停灌后模型组MDA、PCO含量明显升高,SOD含量降低,而给药组MDA、PCO的含量较模型组减少(P<0.01),且减少SOD含量的降低(P<0.01)。说明缺血再灌注能够增加心脏的氧化应激,诱导氧化损伤,CAPE保护可以减少氧化损伤,且呈剂量依赖性。结论咖啡酸苯乙酯对大鼠离体心脏缺血再灌注损伤具有保护作用,其机制可能与抗氧化作用有关。
OBJECTIVE: To establish a rat model of myocardial ischemia-reperfusion in vitro and to investigate the protective effect of caffeic acid phenethyl ester on myocardial ischemia-reperfusion injury in vitro. Methods Thirty male Sprague-Dawley rats were randomly divided into Langendorff group and control group. The experiment group was divided into five groups: blank group: KH (Krebs-Henseleit) solution for 100 min; model group: , And reperfusion KH solution for 40 min. Administration group: KH fluid for 30 min, then stopped for 30 min, then rehydrated with KH solution of 3, 6 and 12 mg / L CAPE for 40 min. In the experiment, the changes of coronary flow, myocardial contractility and heart rate in isolated rat hearts were observed. After stopping irrigation, the contents of malondialdehyde (MDA), protein carbonylation (PCO) and superoxide dismutase (SOD) in each group were measured. Results During the reperfusion period, the contractility of the model group was weakened, the tension increased, the heart rate slowed down, the coronary flow rate decreased obviously, and the arrhythmia appeared. The contractility, tension and heart rate of the model group increased after reperfusion Pulse flow increased significantly, rhythm and tidy. After stopping irrigation, the content of MDA and PCO in the model group increased significantly and the content of SOD decreased, while the content of MDA and PCO in the model group decreased (P <0.01) and decreased the content of SOD (P <0.01). Ischemia-reperfusion can increase oxidative stress in the heart and induce oxidative damage. CAPE protects against oxidative stress in a dose-dependent manner. CONCLUSION Caffeic acid phenethyl ester has a protective effect on ischemia-reperfusion injury in isolated rat hearts. The mechanism may be related to anti-oxidative effects.