Hydrogen-rich medium suppresses the generation of reactive oxygen species, elevates the Bcl-2/Bax ratio and inhibits advanced glycation end product-induced apoptosis.
Hong Jiang, Pan Yu, De-Hui Qian, Zhe-Xue Qin, Xue-Jun Sun, Jie Yu, Lan Huang · International journal of molecular medicine · 2013
Research-use notice
Independent study record
Each H2HUBB study page organizes source-linked research details for educational use. Interpretation should remain proportional to the study design, population, controls, and limitations.
H2HUBB TAKEAWAY
In Sprague-Dawley rats, the purpose of the present study was to determine whether using hydrogen-rich medium (HRM) to increase hydrogen levels in endothelial cells (ECs) protects ECs from apoptosis induced by advanced glycation end products (AGEs). These results are preclinical and suggest molecular hydrogen's therapeutic potential in the condition studied. Further human research is needed to establish clinical effectiveness.
What the Researchers Studied
The study examined sprague-Dawley rats.
How Molecular Hydrogen Was Used
The purpose of the present study was to determine whether using hydrogen-rich medium (HRM) to increase hydrogen levels in endothelial cells (ECs) protects ECs from apoptosis induced by advanced glycation end products (AGEs). , hydrogen exhibits significant protective effects against AGE-induced EC injury possibly through reducing ROS generation, intracellular antioxidant enzyme system protection and elevation of the Bcl-2/Bax ratio.
What the Researchers Found
The purpose of the present study was to determine whether using hydrogen-rich medium (HRM) to increase hydrogen levels in endothelial cells (ECs) protects ECs from apoptosis induced by advanced glycation end products (AGEs).
H₂ Mechanisms / Biological Findings
The source material reviewed did not establish a specific molecular hydrogen mechanism for the reported findings.
Authors’ Conclusion
The authors concluded that , hydrogen exhibits significant protective effects against AGE-induced EC injury possibly through reducing ROS generation, intracellular antioxidant enzyme system protection and elevation of the Bcl-2/Bax ratio.