Hydrogen-rich saline alleviates inflammation and apoptosis in myocardial I/R injury via PINK-mediated autophagy.
Li Yao, Hongguang Chen, Qinghua Wu, Keliang Xie · International journal of molecular medicine · 2019
Research-use notice
Independent study record
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H2HUBB TAKEAWAY
The results demonstrated that treatment with hydrogen improved the myocardial infarction size of hearts, cardiac function, apoptosis and cytokine release following MI/R in rats. The authors concluded that in summary, the present study indicated that treatment with hydrogen‐rich saline improved the inflammatory response and apoptosis in MI/R via PINK1/Parkin‐mediated mitophagy. These findings come from a laboratory model and suggest molecular hydrogen's biological potential. Further research is needed to determine clinical relevance.
What the Researchers Tested
In vitro cell-culture laboratory experiment.
Laboratory Model
MI/R injury was performed by surgical ligation of the left coronary artery in vivo and H9C2 cell injury was performed by hypoxia/reoxygenation (H/R) in vitro.
How Molecular Hydrogen Was Used
Hydrogen‐rich saline was administered twice through intraperitoneal injection at a daily dose of 10 ml/kg following the operation in the in vivo model, and hydrogen‐rich medium culture was used for cells instead of normal medium in vitro.
What Molecular Hydrogen Changed
The results demonstrated that treatment with hydrogen improved the myocardial infarction size of hearts, cardiac function, apoptosis and cytokine release following MI/R in rats.
Proposed Mechanism
In summary, the present study indicated that treatment with hydrogen‐rich saline improved the inflammatory response and apoptosis in MI/R via PINK1/Parkin‐mediated mitophagy. Hydrogen exerts an effective therapeutic role in numerous diseases associated with I/R injury via its anti‐inflammation, anti‐apoptosis and anti‐oxidative properties. Therefore, the present study investigated the effect of hydrogen on the myocardial inflammation response and apoptosis in myocardial ischemic/reperfusion (MI/R) injury, and further explored the mechanism of PTEN‐induced kinase 1 (PINK1)/Parkin‐induced mitophagy in the protection of hydrogen on MI/R injury.
Authors’ Conclusion
These findings come from a laboratory model and suggest molecular hydrogen's biological potential. Further research is needed to determine clinical relevance.