Abstract
Background Oxidative stress and autophagy both play key roles in continuous cardiomyocyte death and cardiac dysfunction after reperfusion therapy for acute myocardial ischemia-reperfusion injury. Coenzyme Q10 (CQ10), which is a fat-soluble quinone antioxidant, is involved in the pathophysiological processes of neurodegenerative diseases, cancer, diabetes, heart failure, and other diseases. Our objective was to determine if, and by what mechanism, CQ10 can ameliorate acute myocardial ischemia-reperfusion injury and improve heart function. Methods and Results Fat-soluble CQ10 in soybean oil solvent was preconditioned in rats with acute myocardial ischemia-reperfusion injury by intraperitoneal injection. Oxidant and antioxidant levels were compared between the preconditioned and control groups. Autophagy was measured by Western blotting analysis of autophagy proteins. Proapoptotic proteins and immunofluorescence were used to assess cell apoptosis. Infarct size was determined by triphenyl tetrazolium chloride (TTC) staining and Evans blue staining and visualized myocardial pathology by tissue staining. Finally, we assessed cardiac function by electrocardiography (ECG) and hemodynamics. Conclusions This study reveals that CQ10 preconditioning regulates antioxidant levels and the oxidant balance, enhances autophagy, reduces myocardial apoptosis and death, and improves cardiac function in rats with acute ischemia-reperfusion injury. These results imply that CQ10 protects against acute myocardial ischemia-reperfusion injury via the antioxidative stress and autophagy pathways.
Highlights
Percutaneous coronary intervention is a principal therapeutic approach for the treatment of acute myocardial infarction, which has threatened the life and health of millions of people in recent years [1]
Because Coenzyme Q10 (CQ10) is a well-known antioxidant agent, we demonstrated that preconditioning with CQ10 significantly increased antioxidant levels of glutathione peroxidase (GPx), glutathione reductase (GR), superoxide dismutase (SOD), and GSH (p < 0 05, n = 6) and decreased oxidant thiobarbituric acid reactive substances (TBARS) levels (p < 0 05, n = 6) in rats with acute myocardial ischemia-reperfusion injury (Table 1)
It has become increasingly clear that the level of oxidants is greatly increased in the postischemic heart, and oxidants play a critical role in postischemic injury
Summary
Percutaneous coronary intervention is a principal therapeutic approach for the treatment of acute myocardial infarction, which has threatened the life and health of millions of people in recent years [1]. Autophagy is an intracellular defense and stress regulation mechanism that works by degrading damaged organelles and denaturing long-lived proteins and nucleic acids to provide raw materials and energy for cell surviving from injury, apoptosis, and death [10, 11]. Oxidative stress and autophagy both play key roles in continuous cardiomyocyte death and cardiac dysfunction after reperfusion therapy for acute myocardial ischemia-reperfusion injury. This study reveals that CQ10 preconditioning regulates antioxidant levels and the oxidant balance, enhances autophagy, reduces myocardial apoptosis and death, and improves cardiac function in rats with acute ischemia-reperfusion injury. These results imply that CQ10 protects against acute myocardial ischemia-reperfusion injury via the antioxidative stress and autophagy pathways
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