CAJ | 학술논문

本文利用冠脉结扎/放松方法和Langendorff灌注技术,建立在体和离体大鼠心脏缺血/再灌注(ischemia/reperfusion,I/R)损伤模型,探讨白藜芦醇甙(polydatin)对大鼠I/R心肌损伤的保护作用及其机制.观察白藜芦醇甙对缺血和再灌注心律失常、心肌梗死面积、心脏收缩功能、心肌超氧化物歧化酶(superoxide dismutase,SOD)活性、丙二醛(malondialdehyde,MDA)含量、NO含量以及一氧化氮合酶(nitric oxide synthase,NOS)活性的影响.结果显示:与对照组相比,白藜芦醇甙组大鼠缺血和再灌注心律失常明显降低(P<0.05,P<0.01);心肌梗死面积显著减少(P<O.01);I/R心脏左心室发展压(left ventricular developedpressure,LVDP)、左心室压力上升和下降最大变化速率(±LVdp/dmax)、冠脉流量(coronary flow,CF)明显改善(P<0.05,P<0.01);心肌SOD活性升高,MDA含量降低(P<0.05);NO含量和NOS及eNOS活性也明显升高(P<0.05);此外,NOS抑制剂L-NAME拮抗白藜芦醇甙对I/R心肌的保护作用.结果提示:白藜芦醇甙具有明显的抗心肌I/R损伤作用,此作用主要由cNOS产生的NO增加所介导.
본문이용관맥결찰/방송방법화Langendorff관주기술,건립재체화리체대서심장결혈/재관주(ischemia/reperfusion,I/R)손상모형,탐토백려호순대(polydatin)대대서I/R심기손상적보호작용급기궤제.관찰백려호순대대결혈화재관주심률실상、심기경사면적、심장수축공능、심기초양화물기화매(superoxide dismutase,SOD)활성、병이철(malondialdehyde,MDA)함량、NO함량이급일양화담합매(nitric oxide synthase,NOS)활성적영향.결과현시:여대조조상비,백려호순대조대서결혈화재관주심률실상명현강저(P<0.05,P<0.01);심기경사면적현저감소(P<O.01);I/R심장좌심실발전압(left ventricular developedpressure,LVDP)、좌심실압력상승화하강최대변화속솔(±LVdp/dmax)、관맥류량(coronary flow,CF)명현개선(P<0.05,P<0.01);심기SOD활성승고,MDA함량강저(P<0.05);NO함량화NOS급eNOS활성야명현승고(P<0.05);차외,NOS억제제L-NAME길항백려호순대대I/R심기적보호작용.결과제시:백려호순대구유명현적항심기I/R손상작용,차작용주요유cNOS산생적NO증가소개도.
The aim of the present study was to investigate the protective effect of polydatin against myocardial ischemia/repeffusioninjury in rats and the underlying mechanism. In anesthetized rats, ischemia and reperfusion arrhythmia produced by ligating and loosingthe coronary artery was recorded and myocardial infarct size was measured. In Langendorff isolated rat heart, cardiac function wasrecorded before and after 30 min of global ischemia followed by 60 rain of reperfusion. The parameters of cardiac function include leftventricular developed pressure (LVDP), maximal differentials of LVDP (±LVdp/dtmax) and coronary flow (CF) were measured. Myocar-dial superoxide dismutase (SOD) activity, the contents of myocardial malondialdehyde (MDA) and nitric oxide (NO) as well as theactivity of nitric oxide synthase (NOS) were measured in isolated heart. The results showed: (1) Axrhythmia score and myocardialinfarct size were significantly lower in polydatin group than that in the control group (P<0.05, P<0.01); (2) The recovery of LVDE±LVdp/dtmax and CF during reperfusion in polydatin group were significantly better than that in the control rats (P<0.05, P<0.01); (3)SOD activity in polydatin group was significantly higher than that in the control group, but MDA content was lower in polydatingroup than that in the control group (P<0.05); (4) NO content and NOS activity, especially constitutive nitric oxide synthase (cNOS)activity in polydatin group were higher than that in the control group (P<0.05); (5) L-NAME, the NOS inhibitor, reversed theprotective effect of polydatin against ischemia/reperfusion injury. The results suggest that polydatin has a protective effect againstischemia/reperfusion injury in rat heart. The cardioprotection of polydatin is mainly mediated by cNOS which leading to an increase inNO production.