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Ginsenoside Rb3 protects cardiomyocytes against hypoxia/reoxygenation injury via activating the antioxidation
Jing Sun1, Xiaohong Yu1, Haiquan Huangpu1
1Second Department of Cardiovascular, First Affiliated Hospital, Heilongjiang University of Chinese Medicine, No. 26, Heping Road, Xiangfang District, Harbin 150040, Heilongjiang Province, PR China.
Objectives:
This study aimed to investigate the pharmacological function and underlying regulation mechanisms of Ginsenoside-Rb3 (G-Rb3) in cardioprotection.
Methods:
Cultured H9C2 cells were pre-treated with gradient concentrations of G-Rb3, and subsequently challenged with hypoxia/reoxygenation (H/R) treatment. The generation of intracellular reactive oxygen species (ROS) and cellular antioxidatant capacity were quantified. Cell apoptosis was measured by flow cytometry. Myocardial ischemia reperfusion injury (MIRI) rat models constructed by coronary artery ligation surgery were orally administrated with G-Rb3 for 5 consecutive days, and then infarction area, apoptosis ratio and total antioxidant capacity (T-AOC) of myocardial tissues were measured. PERK phosphorylation inhibitor GSK2656157 and Nrf2 translocation inhibitor ML385 were co-treated with G-Rb3 to further verify the signaling pathway mediated by G-Rb3.
Results:
H/R treatment induced prominent ROS deposition and elevated cell apoptosis ratio in H9C2 cells. G-Rb3 pretreatment suppressed intracellular ROS accumulation and enhanced T-AOC, partially rescuing cardiomyocytes from oxidative stress and apoptosis induced by H/R. In vivo, the cardiac infarction area of MIRI model rats was reduced by G-Rb3 treatment via improved total antioxidant levels. In the further functional and mechanistic studies, G-Rb3 was found to induce PERK phosphorylation and nuclear translocation of transcriptional factor Nrf2, promoting the expression of antioxidative genes such as HMOX1. Inhibitors GSK2656157 and ML385 reversed the effects of G-Rb3.
Conclusion:
Our studies revealed a novel mechanism of G-Rb3 to attenuates oxidative stress via activating the antioxidation signaling pathway of PERK/Nrf2/HMOX1 in vivo and in vitro, which may help us to enrich the theoretical knewledge of Ginsenoside-Rb3 in cardiopretection.
Insights
Ginsenoside-Rb3 (G-Rb3) protects the heart by reducing oxidative stress and apoptosis. It activates the PERK/Nrf2/HMOX1 pathway, offering a novel cardioprotective mechanism.
Area of Science:
- Cardiovascular Pharmacology
- Molecular Biology
- Natural Product Chemistry
Background:
- Oxidative stress and apoptosis are key contributors to myocardial ischemia reperfusion injury (MIRI).
- Ginsenoside-Rb3 (G-Rb3) is a promising natural compound with potential cardioprotective effects.
- Understanding the precise mechanisms of G-Rb3 in cardioprotection is crucial for therapeutic development.
Purpose of the Study:
- To investigate the pharmacological function of Ginsenoside-Rb3 (G-Rb3) in cardioprotection.
- To elucidate the underlying regulatory mechanisms of G-Rb3 in mitigating cardiac injury.
- To explore the role of the PERK/Nrf2/HMOX1 signaling pathway in G-Rb3-mediated cardioprotection.
Main Methods:
- H9C2 cells and MIRI rat models were used to assess G-Rb3's effects.
- Key parameters measured included reactive oxygen species (ROS), total antioxidant capacity (T-AOC), and apoptosis.
- Signaling pathway activation was confirmed using specific inhibitors (GSK2656157, ML385).
Main Results:
- G-Rb3 treatment reduced ROS accumulation and apoptosis in H9C2 cells under hypoxia/reoxygenation (H/R).
- In MIRI rats, G-Rb3 decreased infarct size and improved antioxidant levels.
- G-Rb3 was shown to induce PERK phosphorylation and Nrf2 nuclear translocation, upregulating antioxidative genes like HMOX1.
Conclusions:
- Ginsenoside-Rb3 exhibits significant cardioprotective effects by attenuating oxidative stress and apoptosis.
- The study reveals a novel mechanism involving the activation of the PERK/Nrf2/HMOX1 signaling pathway.
- These findings enrich the understanding of G-Rb3's therapeutic potential in cardiovascular diseases.
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