Molecular hydrogen protects against ischemia-reperfusion injury in a mouse fatty liver model via regulating HO-1 and Sirt1 expression.
Shaowei Li, Masayuki Fujino, Naotsugu Ichimaru, Ryosuke Kurokawa, Shinichi Hirano, Lisha Mou, Shiro Takahara, Terumi Takahara, Xiao-Kang Li · Scientific reports · 2018
Research-use notice
Independent study record
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H2HUBB TAKEAWAY
In contrast, H₂ treatment significantly suppressed the signs of I/R injury in fatty liver. 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
Primary hepatocytes and Kupffer cells (KCs) were obtained from fatty liver and subjected to hypoxia/reoxygenation.
How Molecular Hydrogen Was Used
Seeking to ameliorate liver injury following I/R in fatty liver, the researchers examined the protective effect of hydrogen (H₂) saline on I/R liver injury in a methionine and choline-deficient plus high fat (MCDHF) diet-induced fatty liver mouse model. Saline containing 7 ppm H₂ was administrated during the process of I/R. Apoptosis-related proteins and components of the signaling pathway were analyzed after treatment with hydrogen gas.
What Molecular Hydrogen Changed
In contrast, H₂ treatment significantly suppressed the signs of I/R injury in fatty liver.
Proposed Mechanism
Apoptosis-related proteins and components of the signaling pathway were analyzed after treatment with hydrogen gas.
Authors’ Conclusion
These findings come from a laboratory model and suggest molecular hydrogen's biological potential. Further research is needed to determine clinical relevance.