The Anti-inflammatory Effect of Hydrogen on Lung Transplantation Model of Pulmonary Microvascular Endothelial Cells During Cold Storage Period.

Abstract

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. Pulmonary microvascular endothelial cells were divided into 4 groups: blank, control, oxygen (O2), and 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 minutes for 4 hours. During the transplantation period, the sealed containers were warmed for 1 hour at room temperature. In the reperfusion period, the containers were aerated with 50% O2, 5% CO2 and 45% N2 at 37°C. The concentrations of interleukin-6 and tumor necrosis factor-α in the extracellular solutions were significantly decreased, and the concentration of interleukin-10 was increased in the H2 group. Intercellular adhesion molecule-1 expression was inhibited by H2. Furthermore, H2 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 H2 administration. 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.