...
  • 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>Cell and Tissue Research >Aloin antagonizes stimulated ischemia/reperfusion-induced damage and inflammatory response in cardiomyocytes by activating the Nrf2/HO-1 defense pathway
【24h】

Aloin antagonizes stimulated ischemia/reperfusion-induced damage and inflammatory response in cardiomyocytes by activating the Nrf2/HO-1 defense pathway

机译：Aloin antagonizes stimulated ischemia/reperfusion-induced damage and inflammatory response in cardiomyocytes by activating the Nrf2/HO-1 defense pathway

获取原文
获取原文并翻译 | 示例
           
页面导航
  • 摘要
  • 著录项
  • 相关主题

摘要

Myocardial ischemia/reperfusion injury (I/RI) frequently incurs in acute myocardial infarction with high morbidity and mortality worldwide and is characterized with cardiomyocyte apoptosis and inflammatory response. Aloin is a major anthraquinone from Aloe species and fulfills pleiotropic protective functions in several disease models including hepatic injury. Nevertheless, the potential of aloin in MI/RI remains elusive. Intriguingly, aloin had modest cytotoxicity in H9c2 cardiomyocytes. Importantly, aloin dose-dependently ameliorated cell viability that was inhibited in response to simulated ischemia/reperfusion (SI/R) stimulation. Moreover, the enhanced apoptosis in cells under SI/R conditions were reduced after aloin treatment, concomitant with the decrease in pro-apoptotic Bax protein levels and increase in anti-apoptotic Bcl-2 protein expression. Of interest, aloin administration attenuated SI/R-induced oxidant stress by decreasing reactive oxygen species (ROS) production, lactate dehydrogenase (LDH), and malondialdehyde (MDA) release and increasing activity of anti-oxidant stress enzyme superoxide dismutase (SOD). Additionally, the elevated pro-inflammatory cytokine levels were counteracted after aloin treatment in cells under SI/R conditions, including TNF-alpha, IL-6, and IL-1 beta. Mechanically, aloin further enforced the activation of the NF-E2-related factor 2 (Nrf2)/heme oxygenase-1 (HO-1) signaling. Noticeably, blockage of this pathway by si-Nrf2 transfection blunted aloin-mediated cardioprotective efficacy against SI/R-evoked oxidative stress injury and inflammatory response. Thus, these findings corroborate that aloin may antagonize SI/R-induced cardiomyocyte injury by attenuating excessive oxidative stress and inflammation, thereby endorsing its potential as a promising therapeutic agent against myocardial infarction.

著录项

获取原文

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