Open Access

MG132 protects against lung injury following brain death in rats

  • Authors:
    • Huijuan Shi
    • Dongjing Yang
    • Zhongkun Huo
    • Yuexia Li
    • Wenzhi Guo
    • Shuijun Zhang
  • View Affiliations

  • Published online on: September 23, 2022     https://doi.org/10.3892/etm.2022.11623
  • Article Number: 687
  • Copyright: © Shi et al. This is an open access article distributed under the terms of Creative Commons Attribution License.

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Abstract

Brain death (BD) results in injury to organs and induces lung donor dysfunction. Since the 20S proteasome abnormality is associated with a variety of diseases, the present study investigated whether it was involved in lung injury following BD in rats, and the effects of the proteasome inhibitor MG132 on lung injury was also assessed. Rats were assigned to a BD group or a control sham group. The BD group of rats were sacrificed at different time points after BD. Administration of MG132 was performed intraperitoneally 30 min before BD. Arterial blood was drawn to measure the oxygenation index [partial artery pressure of oxygen (PaO2)/fractional concentration of inspired oxygen (FiO2)]. The right lung was used for staining with hematoxylin and eosin, immunohistochemistry, immunofluorescence, western blotting and RT‑qPCR analysis. The left lung was used to measure the wet and dry weights. Rat alveolar macrophages (NR8383) were treated with MG132 and hypoxia/reoxygenation (H/R) and used for western blotting and flow cytometry. The PaO2/FiO2 ratio decreased after BD; the wet/dry weight ratio, histological lung injury score and protein expression of 20S proteasome β1 and inducible nitric oxide synthase (iNOS) gradually increased in rats after BD. Colocalization in the immunofluorescence between 20S proteasome β1 and iNOS was observed. MG132 treatment increased the PaO2/FiO2 ratio and decreased the wet/dry weight ratio, histological lung injury score and protein expression of 20S proteasome β1 and iNOS in rats after BD. MG132 was revealed to increase NR8383 apoptosis after H/R and to upregulate the protein expression levels of p‑JNK and cleaved‑caspase 3. Overall, the proteasome inhibitor MG132 could effectively reduce lung injury, which may be associated with its ability to inhibit the expression of the proteasome and promote the apoptosis of alveolar macrophages.
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November-2022
Volume 24 Issue 5

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Spandidos Publications style
Shi H, Yang D, Huo Z, Li Y, Guo W and Zhang S: MG132 protects against lung injury following brain death in rats. Exp Ther Med 24: 687, 2022
APA
Shi, H., Yang, D., Huo, Z., Li, Y., Guo, W., & Zhang, S. (2022). MG132 protects against lung injury following brain death in rats. Experimental and Therapeutic Medicine, 24, 687. https://doi.org/10.3892/etm.2022.11623
MLA
Shi, H., Yang, D., Huo, Z., Li, Y., Guo, W., Zhang, S."MG132 protects against lung injury following brain death in rats". Experimental and Therapeutic Medicine 24.5 (2022): 687.
Chicago
Shi, H., Yang, D., Huo, Z., Li, Y., Guo, W., Zhang, S."MG132 protects against lung injury following brain death in rats". Experimental and Therapeutic Medicine 24, no. 5 (2022): 687. https://doi.org/10.3892/etm.2022.11623