Scholarlink

<p>Acute kidney injury (AKI) has become a disease of global concern due to its high morbidity and mortality. This has highlighted the need for renoprotective agents. <i>Astragaloside IV (AS-IV)</i> is a saponin isolated from Astragalus membranaceus with good antioxidant, anti-inflammatory and anti-tumor properties. In this study, HK2 cells and rat model were utilized to explore the protective effect of <i>AS-IV</i> against cadmium chloride-induced oxidative stress-induced apoptosis. CdCl<sub>2</sub>-induced apoptosis, ROS production, and mitochondrial membrane potential alterations were significantly inhibited in <i>AS-IV</i> -treated HK2 cells. Expression of the mitochondria-associated apoptotic proteins Cleaved-Caspase3, Cleaved-Caspase9, and Cleaved-PARP was significantly reduced after <i>AS-IV</i> intervention. In addition, <i>AS-IV</i> inhibited Rat weight loss and also alleviated the symptoms of CdCl<sub>2</sub>-induced nephrotoxicity in a rat model of CdCl<sub>2</sub>-induced kidney injury. Further experiments showed that <i>AS-IV</i> suppresses heavy metal Cd-induced mitochondria-mediated apoptosis by regulating the Nrf2/HO-1 pathway. In conclusion, <i>AS-IV</i> could protect the kidney from heavy metal-induced toxicity and could be used as a nephroprotective agent.</p>

错误：搜索内容不能为空，请输入英文关键词
错误：关键词超出字数限制，请精简
高级检索

Astragaloside IV attenuates cadmium induced nephrotoxicity in rats by activating Nrf2

  • 期刊论文

  • 出版模式：

    开放获取

  • 发表日期：

    2025年1月15日

查看全文
  • Yuchen Li,
  • Jiayi Zhou,
  • Tianxin Zhang,
  • Xiaocong Li,
  • Cheng Wu,
  • Ziyi Zhao,
  • Jianyuan Tang,
  • Xiaoyu Tan,
  • Qiongying Hu,
  • Wenhao Liao

摘要

Acute kidney injury (AKI) has become a disease of global concern due to its high morbidity and mortality. This has highlighted the need for renoprotective agents. Astragaloside IV (AS-IV) is a saponin isolated from Astragalus membranaceus with good antioxidant, anti-inflammatory and anti-tumor properties. In this study, HK2 cells and rat model were utilized to explore the protective effect of AS-IV against cadmium chloride-induced oxidative stress-induced apoptosis. CdCl2-induced apoptosis, ROS production, and mitochondrial membrane potential alterations were significantly inhibited in AS-IV -treated HK2 cells. Expression of the mitochondria-associated apoptotic proteins Cleaved-Caspase3, Cleaved-Caspase9, and Cleaved-PARP was significantly reduced after AS-IV intervention. In addition, AS-IV inhibited Rat weight loss and also alleviated the symptoms of CdCl2-induced nephrotoxicity in a rat model of CdCl2-induced kidney injury. Further experiments showed that AS-IV suppresses heavy metal Cd-induced mitochondria-mediated apoptosis by regulating the Nrf2/HO-1 pathway. In conclusion, AS-IV could protect the kidney from heavy metal-induced toxicity and could be used as a nephroprotective agent.