首页> 美国卫生研究院文献>Evidence-based Complementary and Alternative Medicine : eCAM >Protective Effects of Shen-Yuan-Dan a Traditional Chinese Medicine against Myocardial Ischemia/Reperfusion Injury In Vivo and In Vitro
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Protective Effects of Shen-Yuan-Dan a Traditional Chinese Medicine against Myocardial Ischemia/Reperfusion Injury In Vivo and In Vitro

机译:中药肾元丹对体内和体外心肌缺血/再灌注损伤的保护作用

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摘要

Objectives. The study was to investigate the effects and mechanisms of Shen-Yuan-Dan (SYD) pharmacological postconditioning on myocardial ischemia/reperfusion (I/R) injury. Methods. In the in vivo experiment, myocardial injury markers and histopathology staining were examined. In the in vitro experiment, cell viability and cell apoptosis were, respectively, detected by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assays and Hoechst 33342 fluorochrome staining. The protein expressions of Bcl-2 and Bax were determined by immunocytochemistry assay. Results. Both low and high doses of SYD protected myocardium against I/R injury in rat model by reducing lactic dehydrogenase (LDH) and creatine kinase-MB (CK-MB) activity and malondialdehyde (MDA) content, increasing superoxide dismutase (SOD) activity and attenuating histopathology injury. Meanwhile, in the in vitro experiment, SYD promoted cell viability and inhibited the cardiomyocyte apoptosis. The level of Bcl-2 protein was restored to the normal level by SYD pharmacological postconditioning. In contrast, the Bax protein level was markedly reduced by SYD pharmacological postconditioning. These effects of SYD were inhibited by . Conclusions. The results of this study suggested that SYD pharmacological postconditioning has protective effects against myocardial I/R injury in both in vivo and in vitro models, which are related to activating the phosphatidylinositol 3-kinase/Akt (PI3K/Akt) pathway.
机译:目标。该研究旨在探讨深渊丹(SYD)药理后处理对心肌缺血/再灌注(I / R)损伤的影响及其机制。方法。在体内实验中,检查了心肌损伤标志物和组织病理学染色。在体外实验中,分别通过3-(4,5-二甲基噻唑-2-基)-2,5-二苯基溴化四溴甲烷(MTT)分析和Hoechst 33342荧光染料染色检测细胞活力和细胞凋亡。用免疫细胞化学法检测Bcl-2和Bax蛋白的表达。结果。低剂量和高剂量SYD均可通过降低乳酸脱氢酶(LDH)和肌酸激酶-MB(CK-MB)活性和丙二醛(MDA)含量,增加超氧化物歧化酶(SOD)活性和减轻组织病理学损伤。同时,在体外实验中,SYD促进细胞活力并抑制心肌细胞凋亡。通过SYD药理后处理,Bcl-2蛋白水平恢复到正常水平。相反,SYD药理后处理可显着降低Bax蛋白水平。 SYD的这些作用被抑制。结论。这项研究的结果表明,SYD药理学后处理在体内和体外模型中均具有针对心肌I / R损伤的保护作用,这与激活磷脂酰肌醇3-激酶/ Akt(PI3K / Akt)途径有关。

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