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Ginsenoside Ro Targets BCAT1/2 to Suppress Ferroptosis: A Novel Therapeutic Strategy for Ischemic Cardioprotection
Jincheng Liu1, Feng Wang2, Juan Bai1
1Department of Pharmacy, Jingmen Central Hospital, Jingmen Central Hospital Affiliated to Jingchu University of Technology, Shenzhen Avenue, Duodao District, Jingmen, Hubei 448000, China.
Abstract:
Ginsenoside Ro, a compound with diverse therapeutic potential, has yet to be explored for its role in myocardial ischemia (MI). Our study employed murine MI models, induced by coronary artery ligation and isoproterenol administration, alongside oxygen glucose-deprivation-injured neonatal rat ventricular myocytes, aiming to reveal the effects of Ro in MI injury and elucidate the underlying mechanisms. These findings demonstrated that Ro significantly enhanced cardiac function, mitigated histopathological damage, and reduced the level of apoptosis. Mechanistically, Ro directly targeted branched-chain aminotransferases 1 and 2 (BCAT1 and BCAT2), augmented enzyme activities, and expression of BCAT1/2, thereby activating the Keap1/Nrf2/HO-1 pathway to suppress cardiac ferroptosis. Furthermore, inhibition of BCAT1/2 effectively abolished Ro's cardioprotective effects. This study not only identifies BCAT1/2 as novel molecular targets of Ro but also reveals a previously unrecognized mechanism for suppressing ferroptosis. These findings underscore Ro's potential as a promising BCAT1/2 agonist and therapeutic candidate for MI, offering new insights into cardiovascular protection and highlighting its clinical significance.
Insights
Ginsenoside Ro protects the heart from myocardial ischemia (MI) by targeting branched-chain aminotransferases (BCAT1/2). This activation suppresses ferroptosis, offering a new therapeutic strategy for cardiovascular protection.
Area of Science:
- Cardiovascular Research
- Molecular Pharmacology
- Cellular Biology
Background:
- Myocardial ischemia (MI) remains a leading cause of cardiovascular disease.
- Ginsenoside Ro (Ro) exhibits therapeutic potential but its role in MI is unexplored.
- Understanding novel mechanisms for cardioprotection is crucial.
Purpose of the Study:
- To investigate the protective effects of Ginsenoside Ro against myocardial ischemia.
- To elucidate the underlying molecular mechanisms of Ro's action in MI.
- To identify potential therapeutic targets for MI treatment.
Main Methods:
- Murine models of myocardial ischemia (coronary artery ligation, isoproterenol).
- Oxygen glucose-deprivation (OGD) injury model in neonatal rat ventricular myocytes.
- Assessment of cardiac function, histopathology, apoptosis, and ferroptosis markers.
- Enzyme activity assays and Western blotting for BCAT1/2 and Keap1/Nrf2/HO-1 pathway components.
Main Results:
- Ginsenoside Ro significantly improved cardiac function and reduced myocardial damage and apoptosis in MI models.
- Ro directly targeted and upregulated branched-chain aminotransferases 1 and 2 (BCAT1/2).
- Activation of BCAT1/2 by Ro led to the suppression of cardiac ferroptosis via the Keap1/Nrf2/HO-1 pathway.
- Inhibition of BCAT1/2 abolished the cardioprotective effects of Ro.
Conclusions:
- Ginsenoside Ro demonstrates significant cardioprotective effects against myocardial ischemia.
- BCAT1/2 are identified as novel molecular targets of Ginsenoside Ro.
- Ro suppresses cardiac ferroptosis through the BCAT1/2-Keap1/Nrf2/HO-1 axis, presenting a new therapeutic avenue for MI.
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