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Abstract
This study aims to investigate the influence of excessive oxidative stress on cardiac injury during acute myocardial ischemia (AMI), with a focus on apoptosis, autophagy, and inflammatory cell infiltration, and to detect the role of hydrogen sulfide (H2S) in this process. We found that SOD1 knockout (KO) mice showed excessive oxidative stress and exacerbated myocardium injury after AMI. Increased apoptosis and inflammation response in the ischemic myocardium contribute to this deterioration, whereas enhanced autophagy plays a protective role. Myocardial inflammation after AMI was much more severe in SOD1 KO mice than in wild-type mice. Pretreatment with the H2S donor NaHS reduced autophagy and apoptosis levels in the ischemic myocardium and alleviated the regional inflammation response in the cardiac tissues of SOD1 KO mice. Moreover, autophagy and apoptosis levels were significantly enhanced in SOD1 knockdown primary neonatal rat cardiomyocytes (NRCMs) under glucose deprivation. Pretreatment with NaHS can partially inhibit this elevation. Taken together, we found that excessive oxidative stress can aggravate cardiac injury during AMI. Exogenous H2S can alleviate cardiac injury during AMI by reducing apoptosis and inflammation response in heart tissues under oxidative stress.
Highlights
Acute myocardial ischemia (AMI) induced by coronary artery occlusion is one of the leading causes of cardiovascular morbidity and mortality worldwide [1,2,3]
The TUNEL assay showed that the percentage of apoptotic cells was significantly higher in AMI mice compared to that in sham-operated controls in both WT and SOD1−/− mice, while the number of apoptotic cells was further increased in SOD1−/− AMI mice than that in WT AMI mice (Figure 1(c))
LC3-II increased further in SOD1-knockdown neonatal rat cardiomyocytes (NRCMs) in the presence of CQ under glucose deprivation (GD) (Figure 4(d)). These results suggested that the oxidative stress in NRCMs induced by SOD1 knockdown increased the autophagy flux under GD
Summary
Acute myocardial ischemia (AMI) induced by coronary artery occlusion is one of the leading causes of cardiovascular morbidity and mortality worldwide [1,2,3]. Acute cardiac ischemia is a multifactorial disease that mainly results in dysfunction of mitochondrial energy metabolism, followed by the initiation of myocardial injury [4, 5]. The main characteristic of impaired mitochondrial metabolism is the production of excessive reactive oxygen species (ROS), including hydrogen peroxide, superoxide, peroxynitrite, and hydroxyl radicals [6,7,8], which are mainly generated from mitochondria [9]. The activity of antioxidant enzymes was decreased in patients suffering from AMI in clinical research [13,14,15]. It is not clear whether people with high ROS levels are susceptible to AMI.
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