The Role of LincRNA-EPS/Sirt1/Autophagy Pathway in the Neuroprotection Process by Hydrogen against OGD/R-Induced Hippocampal HT22 Cells Injury.
Ya-Hong Li, Shun Zhang, Lu Tang, Jianguo Feng, Jing Jia, Ye Chen, Li Liu, Jun Zhou · Journal of personalized medicine · 2023
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
The results demonstrated that H₂ attenuated HT22 cell injury, which would be confirmed by the improved cell survival rate and decreased levels of lactate dehydrogenase. The authors concluded that in summary, the study highlighted the crucial function of the lincRNA-EPS/Sirt1/autophagy-dependent pathway in the attenuation impact of H₂ on OGD/R-triggered injury in hippocampal neurons. These findings from a laboratory model add evidence supporting molecular hydrogen's biological and therapeutic potential in the model studied.
What the Findings Mean
H2HUBB reviewed how hydrogen-rich medium affected the outcomes measured in HT22 cells and an oxygen-glucose deprivation/reoxygenation (OGD/R) model were used to mimic CI/R injury in vitro. The results demonstrated that H₂ attenuated HT22 cell injury, which would be confirmed by the improved cell survival rate and decreased levels of lactate dehydrogenase.
What the Researchers Studied
The researchers studied HT22 cells and an oxygen-glucose deprivation/reoxygenation (OGD/R) model were used to mimic CI/R injury in vitro. The study used a in vitro cell-culture laboratory experiment. The comparison condition was control condition or baseline measurements.
What Effects Did Molecular Hydrogen Have?
The procedure for creating a hydrogen-rich medium has already been detailed [ 36 ]. In brief, hydrogen was dissolved in a DMEM at a pressure of 0.4 MPa. Then, the concentration of hydrogen in the solution was determined using a hydrogen electrode, and when the H₂ concentration reached 0.6 mmol/L, the preparation of a medium enriched with hydrogen was completed. The results demonstrated that H₂ attenuated HT22 cell injury, which would be confirmed by the improved cell survival rate and decreased levels of lactate dehydrogenase. The authors concluded that in summary, the study highlighted the crucial function of the lincRNA-EPS/Sirt1/autophagy-dependent pathway in the attenuation impact of H₂ on OGD/R-triggered injury in hippocampal neurons. After treatment with hydrogen, the cell survival rate increased, and the LDH level, apoptosis rate, levels of pro-inflammatory factors, and autophagic rate were remarkably reduced, demonstrating that H₂ could improve the neuronal OGD/R injury by suppressing autophagy. An earlier research report illustrated that hydrogen reduces hepatocyte apoptosis by stimulating the HO-1/Sirt1 pathway in the hepatic I/R injury model [ 26 ].
Why These Findings Matter
These findings from a laboratory model add evidence supporting molecular hydrogen's biological and therapeutic potential in the model studied.
How Strong Is This Evidence?
This is laboratory evidence from a in vitro cell-culture laboratory experiment. It is most informative for the biological mechanisms, cellular responses, or biochemical outcomes directly measured.
Technical Study Details
H2HUBB classifies this publication as laboratory study with laboratory or cellular evidence. The research population or model was HT22 cells and an oxygen-glucose deprivation/reoxygenation (OGD/R) model were used to mimic CI/R injury in vitro. The study used a in vitro cell-culture laboratory experiment. The hydrogen delivery method was hydrogen-rich medium.
Limitations and Safety
No separate limitations or safety findings were identified in the current-study source text available to H2HUBB.
Original Study and H2HUBB Research Context
H2HUBB presents this source-grounded research record as one contribution to the broader molecular-hydrogen evidence base.