General Research
Model: in_vitro
The Anti-inflammatory Effect of Hydrogen on Lung Transplantation Model of Pulmonary Microvascular Endothelial Cells During Cold Storage Period
Simplified Version Available
How Hydrogen Gas May Improve Lung Transplant Success
Researchers in China found that hydrogen gas may improve lung transplant success by reducing cell damage during the cold storage period. The study used a cell culture model to simulate lung transplantation and found that hydrogen gas had an anti-inflammatory effect. This discovery could give hope to people waiting for a lung transplant.
Read Simplified ArticleAbstract
Publish Year 2018 Country China Rank Positive Journal Transplantation Primary Topic Lung Secondary TopicSurgery/Transplantation Model Cell Culture Tertiary TopicTransplantation/Graft Injury Vehicle Gas pH N/A Application Ventilation Comparison Complement
Background
Methods: PMVECs were divided into 4 groups: Blank, Control, Oxygen (O2), and Hydrogen (H2). The Blank group included PMVECs without treatment. During the cold storage period, the O2 group was aerated with 40% O2 and 60% N2, and the H2 group was aerated with 3% H2, 40% O2 and 57% N2. The Control group was aerated without gases. The mixed gases were replaced every 20 min for 4 h. During the transplantation period, the sealed containers were warmed for 1 h at room temperature. In the reperfusion period, the containers were aerated with 50% O2, 5% CO2 and 45% N2 at 37 °C.
Methods
Results: The concentrations of IL-6 and TNF-α in the extracellular solutions were significantly decreased, and the concentration of IL-10 was increased in the H2 group. ICAM-1 expression was inhibited by hydrogen. Furthermore, hydrogen decreased the activation of NF-κB and phosphorylation level of p38. Cell apoptosis was alleviated. The pathological changes in the cell and mitochondria were alleviated after hydrogen administration.
Results
Conclusion: Hydrogen attenuated inflammatory response in a PMVECs lung transplantation model during cold storage. The effect may be achieved by inhibition of p38 MAPK and NF-κB pathways.