This study aimed to observe the mechanism of hydrogen (H2) in a lung transplantation model simulated by pulmonary microvascular endothelial cells (PMVECs), which were divided into 5 groups. The blank group was the normal PMVECs. During cold ischemia period, PMVECs in the control, O2, or H2 groups were aerated with no gas, O2, or 3% H2, and 3% H2 after transfected with a small interfering RNA targeting Nrf2 in the H2+si-Nrf2 group. Treatment with O2 and H2 decreased the oxidative stress injury, inflammation, cell apoptosis, and attenuated energy metabolism compared with the control group (P < 0.05). And the H2 group showed a better outcome with the increased protein expression of the Nrf2 and HO-1, which were conversed in the H2+si-Nrf2 group. In conclusion, H2 attenuated inflammation, oxidative stress injury, cell apoptosis, and maintained the balance between energy supply and demand in a rat PMVECs lung transplantation model via Nrf2/HO-1.
Keywords: Hydrogen; Ischemia-reperfusion injury; Lung transplantation; Nrf2/HO-1 pathway; PMVECs.
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