AIM To investigate the protective effect of polydatin on ischemia-reperfusion (I-R) injury in cardiac muscle and the possible mechanism. METHODS Langendorff technique was used to make I-R injury in rats. Male Sprague-Dawley rats were randomly divided into control, model, polydatin(25, 50 and 75 μmol·L-1), glibenclamide(Gli, 10 μmol·L-1)+polydatin(50 μmol·L-1), 5-hydroxydecanoate(5-HD, 100 μmol·L-1)+polydatin(50 μmol·L-1), and atractyloside (Atr, 20 μmol·L-1)+polydatin(50 μmol·L-1) groups. The hearts in control group were perfused with K-H solution for 110 min. Model group hearts were subjected to 30 min no-flow global ischemia followed by 60 min of reperfusion. The hearts in 3 polydatin groups were perfused with K-H solution containing different concentrations of polydatin for 10 min before I-R. The hearts in Gli+polydatin and 5-HD+polydatin groups were perfused with K-H solution containing Gli or 5-HD for 5 min firstly, then perfused with K-H solution containing both polydatin and Gli or 5-HD for 10 min before I-R. The hearts in Atr+polydatin group were perfused with K-H solution containing polydatin for 10 min before I-R and perfused with K-H solution containing Atr for 15 min after I-R. The cardiac function, including left ventricular end-diastolic pressure (LVEDP), left ventricular developed pressure (LVDP), the maximal rates of rise and decline of left ventricular pressure (±dp/dtmax), and coronary flow (CF), were recorded before, after 30 min no-flow global ischemia and, during 60 min reperfusion. Myocardial infarct size was assessed using 2, 3, 5-triphenyltetrazolium chloride method and myocardial ultrastructure was observed via transmission electron microscope after 60 min reperfusion. RESULTS There were no significant differences in cardiac functional parameters between control and model groups in pre-ischemia condition. Compared with model group, polydatin promoted a better recovery of cardiac function after I-R in a concentration-dependent manner. After 60 min of reperfusion, the values of LVDP, ±dp/dtmax and CF in polydatin groups were much higher, but LVEDP was lower than those in model group. Polydatin (50 μmol·L-1) also significantly reduced myocardial infarct size and relieved the I-R injury of myocardial ultrastructure. The protective effects of polydatin (50 μmol·L-1) on LVDP, LVEDP, ±dp/dtmax and CF, as well as the inhibitory effect on infarct size after I-R were abolished by Gli, 5-HD and Atr. CONCLUSION Polydatin has protective effect against I-R injury in rat hearts, which may be related with the opening of ATP-sensitive potassium channel located in both cell membrane and mitochondrial membrane, as well as inhibition of mitochondrial permeability transition pore opening.%目的 探讨白藜芦醇苷(Poly)对大鼠缺血再灌注(I-R)心肌损伤的保护作用及其机制.方法 应用Langendorff室技术制备离体大鼠心脏I-R损伤模型.雄性SD大鼠随机分为对照组、模型组、Poly(25, 50和75 μmol·L-1)组、格列本脲(Gli)+Poly组、5-羟基癸酸(5-HD)+Poly组和苍术苷(Atr)+Poly组.对照组心脏由K-H液灌流110 min;模型组由K-H液灌流20 min后, 停灌30 min, 复灌60 min;Poly组在I-R处理前用含不同浓度Poly的K-H液灌流10 min;Gli+Poly和5-HD+Poly组在I-R前分别用含Gli (10 μmol·L-1)和5-HD(100 μmol·L-1)的K-H液灌流5 min,再加入Poly (50 μmol·L-1)灌流10 min;Atr+Poly组用含Poly(50 μmol·L-1)K-H液灌流10 min及停灌30 min后,先用含Atr(20 μmol·L-1)的K-H液灌流15 min, 然后改用K-H液灌流.分别记录各组停灌前、停灌30 min和复灌60 min内的左心室舒张末压(LVEDP)、左心室舒张压(LVDP)、左心室等容期压力最大变化速率(±dp/dtmax)和冠脉流量(CF)等心功能指标.心脏复灌60 min后,用氯化三苯基四氮唑染色法测定心肌梗死面积,透射电镜下检测心肌超微结构变化.结果 缺血前各组心功能参数无明显变化.与模型组相比,Poly可浓度依赖性地促进大鼠I-R后心功能的恢复,预防I-R损伤.复灌60 min后,Poly组大鼠心脏LVDP,±dp/dtmax和CF明显高于模型组;LVEDP则低于模型组;缺血前给予Poly(50 μmol·L-1)10 min可明显减小I-R后心肌梗死面积, 并改善心肌超微结构.Gli, 5-HD和Atr可阻断Poly对I-R心脏心功能参数和心肌梗死面积等的保护作用.结论 Poly具有明显的抗心肌I-R损伤作用,其心脏保护作用可能与其增加细胞膜和线粒体膜ATP敏感性钾通道开放和抑制线粒体通透转换孔开放有关.
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