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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75μmol.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60min;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 (10μmol.L-1)和5-HD(100μmol.L-1)的K-H液灌流5 min,再加入Poly (50μmol.L-1)灌流10 min;Atr +Poly组用含Poly(50μmol.L-1)K-H液灌流10 min及停灌30 min后,先用含Atr(20μmol.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(50μmol.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。
Objective To investigate the protective effect of polydatin on myocardial ischemia-reperfusion (I-R) injury in rats and its mechanism. Methods The rat heart I-R injury model was established by Langendorff chamber technique. Male SD rats were randomly divided into control group, model group, Poly (25, 50, and 75 μmol.L-1) group, glibenclamide (Gli) + Poly group, 5-hydroxydecanoic acid (5-HD) + Poly Group and Atractorin (Atr) + Poly group. The control group was perfused with KH solution for 110 min; the model group was perfused with KH solution for 20 min, followed by rest for 30 min and re-instilled for 60 min; Poly group was perfused with KH solution containing different concentrations of Poly for 10 min before IR treatment; Gli + Poly In the 5-HD+Poly group, the KH solution containing Gli (10 μmol.L-1) and 5-HD (100 μmol.L-1) was perfused for 5 min before the addition of the poly (50 μmol.L-1) perfusion. 10 min; Atr + Poly group was perfused with Poly (50 μmol.L-1) KH for 10 min and stopped for 30 min, then perfused with Atr (20 μmol.L-1) KH solution for 15 min, then switched to use. KH liquid perfusion. The left ventricular end-diastolic pressure (LVEDP), left ventricular diastolic pressure (LVDP), left ventricular pressure and the maximum rate of change of left ventricular isovolumic pressure (±dp/dtmax) were recorded before stopping irrigation, 30 minutes of stopping irrigation and 60 minutes of receiving irrigation. ) and coronary flow (CF) and other cardiac function indicators. After 60 min of cardiac reperfution, myocardial infarct size was measured by triphenyltetrazolium chloride staining, and myocardial ultrastructure was detected by transmission electron microscopy. Results There was no significant change in cardiac function parameters before ischemia. Compared with the model group, Poly can promote the recovery of cardiac function after rat I-R in a dose-dependent manner and prevent I-R injury. After 60 min of re-irrigation, the LVDP,±dp/dtmax and CF in the hearts of the Poly group were significantly higher than those in the model group; the LVEDP was lower than that in the model group; Poly(50 μmol.L-1) given 10 min before ischemia could be significantly decreased. After IR, myocardial infarct size and improve myocardial ultrastructure. Gli, 5-HD and Atr can block the protective effect of Poly on I-R heart function parameters and myocardial infarct size. Conclusions Poly has significant anti-myocardial I-R injury, and its cardioprotective effects may be related to the increase of ATP-sensitive potassium channel opening in cell membrane and mitochondrial membrane and inhibition of mitochondrial permeability transition pore opening.