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

IF 1.5 4区 生物学 Q4 CELL BIOLOGY
Qian-Hui Li, Jun-Xian Shen, Shuai-Lei Xu, Kang-Zhen Zhang
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引用次数: 0

Abstract

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.

人参皂苷Rg1通过抑制nlrp3介导的焦亡来减轻心肌缺血再灌注损伤。
核苷结合寡聚化结构域样受体家族含pyrin结构域3 (NLRP3)炎性体的激活和焦亡对心肌缺血/再灌注(I/R)损伤起关键作用。据报道,人参皂苷Rg1 (Rg1)具有多种药理作用。然而,Rg1在焦亡情况下治疗心肌I/R损伤的心脏保护潜力和潜在机制尚未得到全面研究。采用阻断左冠状动脉前降支30 min,再灌注120 min的方法建立大鼠心肌I/R损伤模型,探讨Rg1对I/R损伤的预防作用及可能的机制。在我们的研究中,NLRP3过表达消除了Rg1的心脏保护作用,Rg1处理改善了心肌功能和组织学形态的变化,并通过减少焦亡相关蛋白来抑制I/ r诱导的细胞毒性和心肌细胞焦亡。这些结果表明,Rg1通过显著抑制NLRP3炎性体的激活,减轻了I/ r诱导的心肌损伤和焦亡,可能为缺血性心脏病的治疗提供新的见解。
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来源期刊
CiteScore
3.70
自引率
4.80%
发文量
96
审稿时长
3 months
期刊介绍: In Vitro Cellular & Developmental Biology - Animal is a journal of the Society for In Vitro Biology (SIVB). Original manuscripts reporting results of research in cellular, molecular, and developmental biology that employ or are relevant to organs, tissue, tumors, and cells in vitro will be considered for publication. Topics covered include: Biotechnology; Cell and Tissue Models; Cell Growth/Differentiation/Apoptosis; Cellular Pathology/Virology; Cytokines/Growth Factors/Adhesion Factors; Establishment of Cell Lines; Signal Transduction; Stem Cells; Toxicology/Chemical Carcinogenesis; Product Applications.
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