Key result
Hydrogen inhalation reduces post-MI infarct size and mitochondrial dysfunction by limiting oxidative stress in rats.
Why the study?
Does hydrogen inhalation reduce myocardial infarct size and improve mitochondrial dysfunction in a rat model of acute myocardial infarction?
Does hydrogen inhalation reduce myocardial infarct size and improve mitochondrial dysfunction in a rat model of acute myocardial infarction?
Hydrogen inhalation reduces acute myocardial infarction damage in a preclinical model by downregulating ROS and upregulating antioxidant proteins, thereby impeding apoptosis via the mitochondrial endogenous pathway.
BACKGROUND: Acute myocardial infarction (AMI) is a deadly cardiovascular disease with no effective solution except for percutaneous coronary intervention and coronary artery bypass grafting. Inflammation and apoptosis of the injured myocardium after revascularization seriously affect the prognosis. Hydrogen possesses anti-inflammatory, anti-oxidative, and anti-apoptotic effects and may become a new treatment for AMI. This study explored the specific mechanism by which hydrogen operates during AMI treatment. METHODS: group received 2% hydrogen inhalation treatment for 3 h/Bid. RESULTS: Myocardial infarct size was evaluated using triphenyl tetrazolium chloride staining. Transmission electron microscopy showed reduced mitochondrial damage compared with the MI group. JC-1 staining, which indicates mitochondrial membrane potential, showed a low red/green fluorescence intensity ratio in the MI group compared to that in the control group, indicating mitochondrial membrane potential loss. After hydrogen inhalation, this ratio increased, suggesting partial recovery of membrane potential. In addition, mitochondrial ATP content, mitochondrial complex I, and mitochondrial complex III activity were significantly decreased in the MI group, which was improved after hydrogen administration. Western blotting analysis showed decreased Cyt-c protein levels in the myocardial mitochondria and increased levels in the cytoplasm of MI rats. Following hydrogen inhalation, the levels of ROS, 8-OHdG, and MDA that could represent oxidative stress injury significantly decreased. Besides, the expression of Cyt-C, Bax, cleaved-caspase-9, and cleaved-caspase-3 in MI group significantly increased, while the Bcl-2, TRX2, SOD2 expression decreased. The expression of these proteins in MI+H2 group was improved compared with the MI group. CONCLUSION: Overall, hydrogen inhalation reduces myocardial infarct size, improves mitochondrial dysfunction, and modulates the levels of apoptosis-related substances. Importantly, Hydrogen reduces acute myocardial infarction damage by downregulating ROS and upregulating antioxidant proteins.
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Pan et al. (2025) studied Acute myocardial infarction. Hydrogen inhalation vs. MI group without hydrogen was evaluated on Myocardial infarct size and mitochondrial function. In rats with myocardial infarction, 2% hydrogen inhalation reduced myocardial infarct size and improved mitochondrial dysfunction by downregulating ROS and upregulating antioxidant proteins.
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