Scholarlink

<p>Nucleotide-binding oligomerisation domain-like receptor family pyrin domain-containing 3 (NLRP3) inflammasome activation and pyroptosis exert the pivotal influence on myocardial ischemia/reperfusion (I/R) injury. Ginsenoside Rg1 (Rg1) reportedly has multiple pharmacological actions. However, the cardioprotective potential and underlying mechanism of Rg1 in treating myocardial I/R injury in the context of pyroptosis have not been comprehensively investigated. A rat model of myocardial I/R injury was established by blocking the left anterior descending coronary artery for 30&#xa0;min followed by reperfusion for 120&#xa0;min. The prevention of Rg1 against I/R-caused damage and the potential mechanisms were explored. In our study, NLRP3 overexpression abolished the cardioprotective effect of Rg1, and Rg1 treatment improved myocardial function and changes in histological morphology and suppressed I/R-induced cytotoxicity as well as cardiomyocyte pyroptosis by reducing the pyroptosis-related proteins. These results indicate that Rg1 mitigated I/R-induced myocardial damage and pyroptosis by dramatically suppressing NLRP3 inflammasome activation and may provide new insights for the treatment of ischemic heart disease.</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

Ginsenoside Rg1 mitigates myocardial ischemia/reperfusion injury by inhibiting NLRP3-mediated pyroptosis

  • 期刊论文

  • 发表日期：

    2025年7月8日

查看全文
  • Qian-Hui Li,
  • Jun-xian Shen,
  • Shuai-lei Xu,
  • Kang-Zhen Zhang

摘要

Nucleotide-binding oligomerisation domain-like receptor family pyrin domain-containing 3 (NLRP3) inflammasome activation and pyroptosis exert the pivotal influence on myocardial ischemia/reperfusion (I/R) injury. Ginsenoside Rg1 (Rg1) reportedly has multiple pharmacological actions. However, the cardioprotective potential and underlying mechanism of Rg1 in treating myocardial I/R injury in the context of pyroptosis have not been comprehensively investigated. A rat model of myocardial I/R injury was established by blocking the left anterior descending coronary artery for 30 min followed by reperfusion for 120 min. The prevention of Rg1 against I/R-caused damage and the potential mechanisms were explored. In our study, NLRP3 overexpression abolished the cardioprotective effect of Rg1, and Rg1 treatment improved myocardial function and changes in histological morphology and suppressed I/R-induced cytotoxicity as well as cardiomyocyte pyroptosis by reducing the pyroptosis-related proteins. These results indicate that Rg1 mitigated I/R-induced myocardial damage and pyroptosis by dramatically suppressing NLRP3 inflammasome activation and may provide new insights for the treatment of ischemic heart disease.