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Traditional Chinese medicine Qili qiangxin inhibits cardiomyocyte apoptosis in rats following myocardial infarction

机译:中药七里强心抑制大鼠心肌梗死后心肌细胞凋亡

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The aim of the present study was to examine the effect of the traditional Chinese medicine Qili qiangxin on cardiomyocyte apoptosis following myocardial infarction (MI) in a rat model. MI was induced in rats by ligation of the anterior descending coronary artery. Survivors were randomly divided into the sham operation, MI, and Qili qiangxin groups (4 g/kg per day). After 28 days, infarction size was measured. In the non-infarcted zones (NIZ), the apoptotic index (AI) was measured by terminal deoxynucleotidyl transferase (TdT)-mediated digoxigenin-conjugated dUTP nick-end labeling (TUNEL). Expression of Fas was detected by immunohistochemistry, and the expression of xanthine oxidase (XO) and caspase-3 by western blot analysis. In addition, the XO and O-2(-), "OH-scavenging activity of myocardial tissue in NIZ was measured by colorimetry. Compared to the MI group, AT and the expression of Fas and caspase-3 were significantly decreased in NIZ. The activity of XO was also considerably reduced while O-2(-) and OH-scavenging activity was significantly increased in the Qili qiangxin group. Ventricular remodeling was attenuated but there were no significant differences in infarct size (IS) or XO expression levels between the Qili qiangxin and MI groups. In conclusion, the results suggest that Qili qiangxin may inhibit cardiomyocyte apoptosis in NIZ in rats. The potential mechanism involved may be associated with its ability to reduce reactive oxygen species (ROS) and to depress the expression of Fas and caspase-3.
机译:本研究的目的是研究中药七里强心对大鼠心肌梗死后心肌细胞凋亡的影响。结扎冠状动脉前降支可诱发大鼠心肌梗死。将幸存者随机分为假手术组,心梗组和七里强心组(每天4 g / kg)。 28天后,测量梗死面积。在非梗死区(NIZ),通过末端脱氧核苷酸转移酶(TdT)介导的洋地黄毒苷缀合的dUTP缺口末端标记(TUNEL)测量凋亡指数(AI)。免疫组织化学法检测Fas的表达,蛋白质印迹法检测黄嘌呤氧化酶(XO)和caspase-3的表达。另外,通过比色法测定NIZ中XO和O-2(-)清除心肌组织的OH。与MI组相比,NIZ中AT以及Fas和caspase-3的表达明显降低。七里强心组的XO活性也显着降低,而O-2(-)和OH清除活性显着增加,心室重构减弱,但梗死面积(IS)或XO表达水平之间无显着差异。结论:七里强新可能抑制大鼠NIZ心肌细胞凋亡,其潜在机制可能与其降低活性氧(ROS)和抑制Fas表达有关。和caspase-3。

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