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Prunasin alleviates OGD/R-induced injury in H9c2 cardiomyocytes via SRC/EGFR-AKT-FoxO-mediated mitochondrial quality
Jiang Li1, Yaoshu Li2, Chengyang Xu3
1Henan Provincial Engineering Research Center of Natural Drug Extraction and Medical Technology Application, Zhengzhou Railway Vocational and Technical College, Zhengzhou 450000, China.
Background:
Myocardial ischemia-reperfusion injury (MIRI) is still difficult to manage clinically, mainly due to limited effective strategies that can simultaneously address oxidative stress, mitochondrial dysfunction and myocardial cell loss. Prunasin is a cyanide glycoside derived from plants of the genus Prunus. Its biological activity has been reported, but its role in ischemia-reperfusion related cardiac injury is not yet clear.
Objectives:
To evaluate the protective effect of prunasin in an oxygen glucose deprivation/reoxygenation (OGD/R) myocardial cell model and explore its potential mechanism.
Methods:
Firstly, potential targets and pathways were explored through network pharmacology and molecular docking. Then, functional validation was performed using H9c2 cells subjected to OGD/R. Evaluated cell viability, LDH release, apoptosis, ROS levels, ATP content, mitochondrial membrane potential and key signaling proteins.
Results:
Network pharmacology highlighted SRC, EGFR and AKT1 as core targets and molecular docking results showed stable binding between prunasin and SRC, supporting this discovery. In experiments, prunasin increased cell viability in a dose-dependent manner and reduced LDH leakage, cell apoptosis and ROS accumulation. Mitochondrial function is also protected, manifested by the recovery of ATP levels and membrane potential. Mechanistically, prunasin activates the SRC/EGFR-AKT-FxO axis, accompanied by enhanced mitochondrial biogenesis, rebalancing of fission/fusion kinetics and increased mitochondrial autophagy, collectively promoting improved mitochondrial quality control under OGD/R stress conditions.
Conclusions:
Prunasin regulates mitochondrial quality control through the SRC/EGFR-AKT-FxO signaling pathway, thereby reducing OGD/R-induced myocardial cell injury, indicating its potential as a candidate drug for myocardial ischemia-reperfusion intervention.
Insights
Prunasin protects heart cells from injury caused by ischemia-reperfusion (MIRI) by improving mitochondrial function via the SRC/EGFR-AKT-FxO pathway. This suggests prunasin
Area of Science:
- Cardiovascular Research
- Molecular Pharmacology
- Mitochondrial Biology
Background:
- Myocardial ischemia-reperfusion injury (MIRI) presents significant clinical challenges due to limited strategies addressing oxidative stress, mitochondrial dysfunction, and cell loss.
- Prunasin, a plant-derived cyanide glycoside, has potential biological activity, but its protective role in cardiac ischemia-reperfusion injury remains uninvestigated.
Purpose of the Study:
- To investigate the protective effects of prunasin on myocardial cells subjected to oxygen-glucose deprivation/reoxygenation (OGD/R).
- To elucidate the underlying molecular mechanisms of prunasin's action in an OGD/R model.
Main Methods:
- Network pharmacology and molecular docking identified core targets (SRC, EGFR, AKT1) and prunasin binding.
- Functional studies utilized H9c2 cells under OGD/R conditions to assess cell viability, LDH release, apoptosis, ROS, ATP, mitochondrial membrane potential, and signaling proteins.
Main Results:
- Prunasin dose-dependently enhanced cell viability, reduced LDH leakage, apoptosis, and ROS levels.
- Mitochondrial function was preserved, evidenced by restored ATP levels and membrane potential.
- Prunasin activated the SRC/EGFR-AKT-FxO axis, promoting mitochondrial biogenesis, balanced fission/fusion, and autophagy for improved quality control.
Conclusions:
- Prunasin mitigates OGD/R-induced myocardial cell injury by regulating mitochondrial quality control via the SRC/EGFR-AKT-FxO pathway.
- These findings highlight prunasin's potential as a therapeutic candidate for myocardial ischemia-reperfusion injury.
