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Published on: January 10, 2025
Hydrogen alleviates myocardial infarction by impeding apoptosis via ROS-mediated mitochondrial endogenous pathway
Shuang Pan1, Bin Wang1, Mengshu Yu1
1Department of Cardiology, The Fourth Affiliated Hospital of Harbin Medical University, Harbin, China.
Insights
Hydrogen inhalation effectively reduces heart damage after acute myocardial infarction (AMI) by improving mitochondrial function and reducing oxidative stress. This treatment offers a promising therapeutic approach for AMI by mitigating inflammation and apoptosis in cardiac tissue.
Area of Science:
- Cardiovascular Research
- Molecular Biology
- Biomedical Engineering
Background:
- Acute myocardial infarction (AMI) poses a significant threat, with limited treatment options beyond revascularization procedures.
- Inflammation and apoptosis post-revascularization negatively impact myocardial recovery.
- Hydrogen's known anti-inflammatory, anti-oxidative, and anti-apoptotic properties suggest therapeutic potential for AMI.
Purpose of the Study:
- To investigate the protective mechanisms of hydrogen therapy in an acute myocardial infarction rat model.
- To elucidate how hydrogen modulates oxidative stress and apoptosis in myocardial tissue.
Main Methods:
- Establishment of a myocardial infarction (MI) rat model by ligating the left anterior descending artery.
- Treatment group received 2% hydrogen inhalation for 3 hours twice daily.
- Assessment of infarct size, mitochondrial function (membrane potential, ATP content, enzyme activity), oxidative stress markers (ROS, 8-OHdG, MDA), and apoptosis-related protein expression (Western blotting).
Main Results:
- Hydrogen inhalation significantly reduced myocardial infarct size and improved mitochondrial function.
- Hydrogen treatment decreased markers of oxidative stress (ROS, 8-OHdG, MDA) and modulated apoptosis-related proteins (e.g., decreased Bax, increased Bcl-2).
- Mitochondrial damage was reduced, and mitochondrial membrane potential was partially restored in the hydrogen-treated group.
Conclusions:
- Hydrogen inhalation mitigates myocardial damage in AMI by reducing infarct size and improving mitochondrial dysfunction.
- The cardioprotective effects of hydrogen are attributed to its ability to downregulate reactive oxygen species (ROS) and upregulate antioxidant proteins.
- Hydrogen demonstrates potential as an effective therapeutic agent for acute myocardial infarction.
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:
Thirty Sprague-Dawley rats were randomly divided into three groups: control, myocardial infarction (MI), and myocardial infarction + hydrogen (MI+H2), each containing 10 rats. The MI rat model was established by ligation of the left anterior descending branch. The MI+H2 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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