Matrine attenuates cardiomyocyte ischemia-reperfusion injury through activating AMPK/Sirt3 signaling pathway

Matrine has been found to affect cell viability and function. In the present study, we explored the cardioprotective role of matrine in cardiomyocyte damage under hypoxia/reoxygenation.In vitro, cardiomyocyte hypoxia/reoxygenation was used to mimic ischemia/reperfusion injury in the presence of matrine. After exposure to hypoxia/reoxygenation, cardiomyocyte viability was reduced and cell apoptosis was increased; this alteration was inhibited by matrine. At the molecular levels, Sirt3 and AMPK were significantly downregulated by hypoxia/reoxygenation injury whereas matrine administration was able to upregulate Sirt3 and AMPK expression and activity in the presence of hypoxia/reoxygenation. Interestingly, inhibition of Sirt3/AMPK pathway abolished the cardioprotective action of matrine on cardiomyocyte in the presence of hypoxia/reoxygenation injury, resulting into cardiomyocyte viability reduction and cell death augmentation. Altogether, our results demonstrated a novel role played by matrine in regulating cardiomyocyte viability and death in the presence of hypoxia/reoxygenation, with a potential application in the clinical practice for the treatment of patients with myocardial infarction.

Automated summary

Matrine demonstrates a cardioprotective effect on cardiomyocyte damage under hypoxia/reoxygenation by upregulating Sirt3 and AMPK expression and activity. Inhibition of the Sirt3/AMPK pathway abolishes this protective action, leading to reduced cardiomyocyte viability and increased cell death. This study suggests a potential therapeutic application of matrine in treating patients with myocardial infarction.