马齿苋总黄酮对缺血再灌注心肌细胞损伤的保护作用

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目的研究马齿苋总黄酮(portulaca total flavone,PTF)对新生大鼠心肌细胞缺血再灌注损伤的保护作用。方法取体外培养的新生大鼠心肌细胞于缺氧24 h复氧1 h造成缺血再灌注(I/R)损伤模型,观察细胞损伤情况,并将PTF终浓度为5、10、20 mg/L分别加入培养基中,预处理24 h后,再置于上述缺氧复氧环境中培养,测定以上不同条件下心肌细胞上清液中的乳酸脱氢酶(LDH)、肌酸激酶(CK)、丙二醛(MDA)、超氧化物歧化酶(SOD)含量,并测定各组细胞内Ca~(2+)浓度。结果与正常对照组相比较,缺血组和再灌组细胞上清液中LDH、CK、MDA含量明显升高(P<0.01),SOD活力则显著降低(P<0.01),缺血组和再灌组细胞内Ca~(2+)浓度均明显升高(P<0.01)。而用PTF预处理后缺血组和再灌组的LDH、CK、MDA显著低于用药前(P<0.01),SOD高于缺血组和再灌组(P<0.01);PTF组(20mg/L)对正常心肌细胞内Ca~(2+)浓度影响小(P>0.05);与PDGF-BB诱导增殖组比较,PTF(5、10、20 mg/L)药物干预组心肌细胞Ca~(2+)浓度明显降低(P<0.05),且存在明显的剂量效应关系。结论 PTF对缺血再灌心肌细胞有保护作用,其作用机制可能与增强抗氧化能力、减轻钙超载有关。 Objective To study the protective effect of portulaca total flavone (PTF) on myocardial ischemia-reperfusion injury in neonatal rats. Methods Rat neonatal rat cardiomyocytes were exposed to hypoxia for 24 hours and reoxygenated for 1 hour to induce ischemia / reperfusion (I / R) injury model. The cell injury was observed. The final concentration of PTF was 5, 10 and 20 mg / L were added to the medium, pretreated for 24 h, then placed in the above hypoxia and reoxygenation culture, measured under different conditions above the cardiomyocyte supernatant lactate dehydrogenase (LDH), creatine kinase (CK ), Malondialdehyde (MDA) and superoxide dismutase (SOD) were measured. Intracellular Ca2 + concentration was measured. Results Compared with the normal control group, the levels of LDH, CK and MDA in the supernatant of the ischemic group and the reperfusion group were significantly increased (P <0.01) and the activities of SOD were significantly decreased (P <0.01) The intracellular Ca2 + concentration in reperfusion group was significantly increased (P <0.01). However, the levels of LDH, CK and MDA in ischemic group and reperfusion group after pretreatment with PTF were significantly lower than those before treatment (P <0.01), and higher than those in ischemic group and reperfusion group (P <0.01) (P <0.05). Compared with the PDGF-BB induced proliferation group, the Ca ~ (2 +) / Ca (superscript 2 + (2+) concentration was significantly lower (P <0.05), and there is a clear dose-response relationship. Conclusions PTF has a protective effect on myocardial cells during ischemia-reperfusion. Its mechanism may be related to the enhancement of anti-oxidation ability and the reduction of calcium overload.
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