This study aimed to observe the mechanism of hydrogen (H) 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, O, or H groups were aerated with no gas, O, or 3% H, and 3% H after transfected with a small interfering RNA targeting Nrf2 in the H+si-Nrf2 group. Treatment with O and H decreased the oxidative stress injury, inflammation, cell apoptosis, and attenuated energy metabolism compared with the control group (P < 0.05). And the H group showed a better outcome with the increased protein expression of the Nrf2 and HO-1, which were conversed in the H+si-Nrf2 group. In conclusion, H 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.
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