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<p>This study aimed to observe the mechanism of hydrogen (H<sub>2</sub>) 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<sub>2</sub>, or H<sub>2</sub> groups were aerated with no gas, O<sub>2</sub>, or 3% H<sub>2</sub>, and 3% H<sub>2</sub> after transfected with a small interfering RNA targeting Nrf2 in the H<sub>2</sub>+si-Nrf2 group. Treatment with O<sub>2</sub> and H<sub>2</sub> decreased the oxidative stress injury, inflammation, cell apoptosis, and attenuated energy metabolism compared with the control group (<i>P</i> &lt; 0.05). And the H<sub>2</sub> group showed a better outcome with the increased protein expression of the Nrf2 and HO-1, which were conversed in the H<sub>2</sub>+si-Nrf2 group. In conclusion, H<sub>2</sub> 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.</p>

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Nrf2/HO-1 Pathway Mediated Protective Effects of Hydrogen in a Model of Lung Transplantation Simulated by Rat Pulmonary Microvascular Endothelial Cells

  • 期刊论文

  • 发表日期：

    2025年1月24日

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  • Bing Zhang,
  • Zhe Li,
  • Chao Meng,
  • Guangchao Zhang,
  • Jiyu Kang,
  • Huacheng Zhou

摘要

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.