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目的:研究虎杖苷(polydatin,PD)对大鼠离体缺血/再灌注(I/R)心肌的保护作用。方法:将40只SD大鼠随机分为4组,包括I/R组,PD(I/R+PD)组,虎杖苷+蛋白激酶C(PKC)阻断剂(I/R+PD+chelerythrine)组和PKC阻断剂(I/R+chelerythrine)组。采用Langendorff灌流法建立离体心肌I/R模型,缺血40 min,再灌注共40 min,分别测量再灌20 min以及再灌40 min时心功能和酶学指标包括:心率、左室收缩压(LVDP)、左室舒张末压(LVEDP)、心室内压最大变化速率(±dp/dtmax)及磷酸激酶(PK)、乳酸脱氢酶(LDH)浓度。结果:心肌I/R可引起心脏功能I/R+PD组±dp/dtmax的恢复率明显回升(P<0.05),同时,LVEDP、LVDP等指标也有明显改善(P<0.05),LDH、PK浓度在复灌20和40 min时明显低于I/R组(P<0.05)。说明PD能部分抑制再灌注期PK和LDH的漏出。PD还能够显著提高I/R心肌的超氧化物歧化酶(SOD)水平,并且降低丙二醛(MDA)水平,发挥心肌保护作用。应用PKC抑制剂chelerythrine则可以消除PD的上述作用。结论:PD可能通过PKC蛋白信号转导通路对I/R心肌发挥保护作用。
Objective: To study the protective effect of polydatin (PD) on myocardial ischemia / reperfusion (I / R) in rats. Methods: Forty Sprague-Dawley rats were randomly divided into four groups: I / R group, PD (I / R + PD) group, PDG + chelerythrine ) Group and PKC blocker (I / R + chelerythrine) group. Langendorff perfusion method was used to establish I / R model of isolated myocardium. After ischemia for 40 min and reperfusion for 40 min, cardiac function and enzymatic parameters including heart rate, left ventricular systolic pressure (LVDP), left ventricular end diastolic pressure (LVEDP), maximum rate of ventricular pressure changes (± dp / dtmax) and phosphokinase (PK) and lactate dehydrogenase (LDH) Results: The recovery rate of ± dp / dtmax in cardiac function I / R + PD group was significantly increased (P <0.05), LVEDP, LVDP and other indexes were significantly improved (P <0.05) The concentration was significantly lower than that of I / R group at 20 and 40 min after reperfusion (P <0.05). PD can partially inhibit the leakage of PK and LDH during reperfusion. PD also significantly increased the level of superoxide dismutase (SOD) in the myocardium of I / R rats, decreased the level of malondialdehyde (MDA) and exerted myocardial protection. The use of chelerythrine, a PKC inhibitor, abrogated the effects of PD. Conclusion: PD may play a protective role in I / R myocardium through PKC protein signal transduction pathway.