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- Title
Ginsenoside Rg3 attenuates myocardial ischemia/reperfusion-induced ferroptosis via the keap1/Nrf2/GPX4 signaling pathway.
- Authors
Zhong, GuoFu; Chen, Junteng; Li, Yangtao; Han, Yue; Wang, Maosheng; Nie, Qinqi; Xu, Mujuan; Zhu, Qinghua; Chang, Xiao; Wang, Ling
- Abstract
Background: Ginsenoside Rg3 is a component of ginseng that protects against myocardial ischemia/reperfusion (MI/R) injury. Ferroptosis is a new form of cell death characterized by oxidative damage to phospholipids. The purpose of this study was to examine the role and of ginsenoside Rg3 in MI/R and the mechanism. Methods: A mouse model of left anterior descending (LAD) ligation-induced myocardial ischemia/reperfusion (MI/R) injury and oxygen-glucose deprivation/reperfusion (OGD/R) were used as in vitro and in vivo models, respectively. Echocardiographic analysis, 2,3,5-triphenyltetrazolium chloride (TTC) staining and hematoxylin-eosin (H&E) staining were used to assess the cardioprotective effects of ginsenoside Rg3. Western blotting, biochemical analysis, small interfering RNA analysis and molecular docking were performed to examine the underlying mechanism. Results: Ginsenoside Rg3 improved cardiac function and infarct size in mice with MI/R injury. Moreover, ginsenoside Rg3 increased the expression of the ferroptosis-related protein GPX4 and inhibited iron deposition in mice with MI/R injury. Ginsenoside Rg3 also activated the Nrf2 signaling pathway. Ginsenoside Rg3 attenuated myocardial ischemia/reperfusion-induced ferroptosis via the Nrf2 signaling pathway. Notably, ginsenoside Rg3 regulated the keap1/Nrf2 signaling pathway to attenuate OGD/R-induced ferroptosis in H9C2 cells. Taken together, ginsenoside Rg3 attenuated myocardial ischemia/reperfusion-induced ferroptosis via the keap1/Nrf2/GPX4 signaling pathway. Conclusions: Our findings demonstrated that ginsenoside Rg3 ameliorate MI/R-induced ferroptosis via the keap1/Nrf2/GPX4 signaling pathway.
- Subjects
RNA analysis; IN vitro studies; COMPUTER-assisted molecular modeling; MYOCARDIAL ischemia; CARRIER proteins; MYOCARDIAL reperfusion complications; PHENOMENOLOGICAL biology; APOPTOSIS; CARDIOTONIC agents; ANIMALS; TRANSCRIPTION factors; CELLULAR signal transduction; IN vivo studies; BIOCHEMISTRY; MICE; EXPERIMENTAL design; OXIDOREDUCTASES; ANIMAL experimentation; WESTERN immunoblotting; GINSENG; ECHOCARDIOGRAPHY; PHARMACODYNAMICS
- Publication
BMC Complementary Medicine & Therapies, 2024, Vol 24, Issue 1, p1
- ISSN
2662-7671
- Publication type
Article
- DOI
10.1186/s12906-024-04492-4