首页> 美国卫生研究院文献>Experimental and Therapeutic Medicine >Traditional Chinese medicine Qili qiangxin inhibits cardiomyocyte apoptosis in rats following myocardial infarction
【2h】

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

代理获取
本网站仅为用户提供外文OA文献查询和代理获取服务,本网站没有原文。下单后我们将采用程序或人工为您竭诚获取高质量的原文,但由于OA文献来源多样且变更频繁,仍可能出现获取不到、文献不完整或与标题不符等情况,如果获取不到我们将提供退款服务。请知悉。

摘要

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 ·O2, ·OH-scavenging activity of myocardial tissue in NIZ was measured by colorimetry. Compared to the MI group, AI and the expression of Fas and caspase-3 were significantly decreased in NIZ. The activity of XO was also considerably reduced while ·O2 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。大鼠结扎冠状动脉前降支可诱发心肌梗死。将幸存者随机分为假手术组,心梗组和七里强新组(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)。免疫组化检测Fas表达,Western blot分析检测黄嘌呤氧化酶(XO)和胱天蛋白酶3的表达。另外,通过比色法测量NIZ中心肌组织的XO和· O2 -· OH清除活性。与MI组相比,NIZ中AI以及Fas和caspase-3的表达显着降低。七里强新组中XO的活性也大大降低,而· O2 -· OH清除活性显着增加。七里强新和心梗组的心室重构减弱,但梗死面积(IS)或XO表达水平无显着差异。总之,结果表明七里强新可能抑制大鼠NIZ中的心肌细胞凋亡。涉及的潜在机制可能与其减少活性氧(ROS)并抑制Fas和caspase-3表达的能力有关。

著录项

相似文献

  • 外文文献
  • 中文文献
  • 专利
代理获取

客服邮箱:kefu@zhangqiaokeyan.com

京公网安备:11010802029741号 ICP备案号:京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有
  • 客服微信

  • 服务号