This paper studies the role of hydrogen in alleviating myocardial infarction by inhibiting the reactive oxygen species (ROS)-mediated mitochondrial intrinsic pathway.
1. Research background: Problem: Acute myocardial infarction (AMI) is a fatal cardiovascular disease, and there is currently no effective solution except percutaneous coronary intervention and coronary artery bypass grafting. Inflammation and apoptosis of damaged myocardium after reperfusion seriously affect prognosis. Difficulty: After myocardial infarction, apoptosis and inflammatory response of cardiomyocytes are the main causes of deterioration of cardiac function and heart failure. It is crucial to find effective anti-inflammatory and antioxidant treatment methods. Related work: Hydrogen may become a new treatment for AMI due to its anti-inflammatory, antioxidant and anti-apoptotic properties. Studies have shown that hydrogen can reduce cerebral ischemia-reperfusion injury and doxorubicin-induced cardiac injury, but its specific mechanism is still unclear. 2. Research methods: Experimental animals: 30 adult healthy male Sprague-Dawley rats, weighing 180±20 g, were used and randomly divided into a control group, a myocardial infarction group (MI), and a myocardial infarction + hydrogen inhalation group (MI+H₂), with 10 rats in each group. Hydrogen inhalation: Rats in the MI+H₂ group inhaled 2% hydrogen for 3 hours a day, twice in a row. Hydrogen was mixed by an air pump and a hydrogen generator, and a hydrogen molecule concentration detector was used to monitor and maintain the hydrogen concentration at 2% in real time. Myocardial infarction model: The myocardial infarction model was established by ligating the left anterior descending branch, and the successful sign was a significant elevation of the ST-T segment of the electrocardiogram and a whitening of the color of the relevant parts of the left ventricle. Detection methods: Triphenyltetrazolium chloride staining was used to evaluate the myocardial infarction area, transmission electron microscopy was used to observe mitochondrial damage, JC-1 staining was used to detect mitochondrial membrane potential, ELISA was used to detect biomarkers in serum and myocardial tissue, Western blotting was used to analyze the expression of related proteins, and immunofluorescence and TUNEL staining were used to detect cell apoptosis. 3. Experimental design: Assessment of myocardial infarction area: The myocardial infarction area in the myocardial infarction group was significantly higher than that in the control group, and the myocardial infarction area in the hydrogen inhalation group decreased by 9.34±0.87% to 25.1±3.25%. Cardiac function assessment: After hydrogen inhalation, the left ventricular ejection fraction (LVEF) and fractional shortening (FS) increased by approximately 23.7% and 14.04%, respectively. Mitochondrial function detection: The mitochondrial ATP content and the activity of mitochondrial complex I and III in the hydrogen inhalation group were significantly higher than those in the myocardial infarction group, and the mitochondrial membrane potential was partially restored. Oxidative stress detection: After hydrogen inhalation, the levels of ROS, 8-OHdG and MDA in myocardial tissue were significantly reduced, and the expression of antioxidant proteins TRX2 and SOD2 was significantly increased. Cell apoptosis detection: The myocardial cell apoptosis in the hydrogen inhalation group was significantly reduced, the expression of Cyt-c, Bax, cleaved-caspase-9 and cleaved-caspase-3 was significantly reduced, and the expression of Bcl-2 was increased. 4. Results and analysis: Hydrogen inhalation significantly reduced myocardial damage and improved cardiac function in rats with myocardial infarction. Hydrogen reduced cardiomyocyte apoptosis by inhibiting the ROS-mediated mitochondrial intrinsic pathway. After hydrogen inhalation, the myocardial infarction area was reduced, cardiac function was improved, mitochondrial damage was alleviated, oxidative stress levels were reduced, and cell apoptosis was reduced. 5. Overall conclusion: Hydrogen inhalation reduced myocardial infarction damage by inhibiting ROS and upregulating the expression of antioxidant proteins. This paper provides new experimental basis for the application of hydrogen in the treatment of myocardial infarction and proposes future research directions, such as further exploring the specific targets of hydrogen and conducting clinical trials.