Abstract:

Background: Lung ischemia-reperfusion injury (LIRI) remains an important factor for the early mortality of lung transplantations. Hydrogen (H2) can attenuate lung injury and improve lung function in animal experiments. In previous studies, pulmonary microvascular endothelial cells (PMVECs) were used to simulate LIRI. We hypothesized that H2 can alleviate inflammatory injury in a PMVECs lung transplantation model in the cold ischemia phase. 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. 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. 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.

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https://doi.org/10.1097/TP.0000000000002276

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