Ginsenoside Rh2 attenuates myocardial ischaemia‑reperfusion injury by regulating the Nrf2/HO‑1/NLRP3 signalling pathway
- Zhi-Xing Fan
- Chao-Jun Yang
- Ya-Hui Li
- Jian Yang
- Cong-Xin Huang
Affiliations: Department of Cardiology, The First College of Clinical Medical Sciences, China Three Gorges University, Yichang, Hubei 443000, P.R. China, Department of Cardiology, Renmin Hospital of Wuhan University, Wuhan, Hubei 430060, P.R. China
- Published online on: November 29, 2022 https://doi.org/10.3892/etm.2022.11734
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Ginsenoside Rh2 (GRh2) is a monomer isolated from red ginseng that has extensive pharmacological effects. However, whether GRh2 has a protective effect on ischaemia/reperfusion (I/R) in the myocardium has yet to be elucidated. The present study aimed to identify the anti‑inflammatory and antioxidant effects of GRh2 on I/R in the myocardium and its underlying mechanism. A rat model of myocardial I/R injury was constructed by ligating the left anterior descending coronary artery, which was subsequently treated with GRh2. A total of 40 male Sprague‑Dawley rats were divided into the following four groups: The sham group, the I/R group, the I/R+GRh2 (10 mg/kg) group and the I/R+GRh2 (20 mg/kg) group. Neonatal rat cardiomyocytes were also used to evaluate the protective effect of GRh2 on hypoxia/reoxygenation (H/R)‑induced myocardial injury in vitro. The GRh2 pre‑treatment reduced the I/R‑ or H/R‑induced release of myocardial enzymes and the production of IL‑1β, IL‑18 and TNF‑α. GRh2 reduced the area of myocardial infarction and the histological changes in the myocardium and improved cardiac functions. In addition, GRh2 reduced the expression levels of NOD‑like receptor family pyrin domain‑containing 3 (NLRP3), apoptosis‑associated speck‑like protein, caspase‑1, malondialdehyde and reactive oxygen species and increased the expression levels of nuclear factor E2‑related factor 2 (Nrf2), heme oxygenase‑1 (HO‑1), glutathione peroxidase and superoxide dismutase. In conclusion, the present study confirmed that GRh2 could reduce oxidative stress and inflammation in cardiomyocytes after reperfusion, and its mechanism of action may be related to its regulation of the Nrf2/HO‑1/NLRP3 signalling pathway.