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Volume 40 Issue 11
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Article Navigation >  CHINESE JOURNAL OF BURNS AND WOUNDS  > 2024  >  40(11): 1034-1042
Zhang H,Guan H,Wang YH,et al.Role and mechanism of ferroptosis in combined burn-blast injury with acute lung injury in rats[J].Chin J Burns Wounds,2024,40(11):1034-1042.DOI: 10.3760/cma.j.cn501225-20240528-00199.
Citation: Zhang H,Guan H,Wang YH,et al.Role and mechanism of ferroptosis in combined burn-blast injury with acute lung injury in rats[J].Chin J Burns Wounds,2024,40(11):1034-1042.DOI: 10.3760/cma.j.cn501225-20240528-00199.
shu

Role and mechanism of ferroptosis in combined burn-blast injury with acute lung injury in rats

doi: 10.3760/cma.j.cn501225-20240528-00199
  • 1.

    Henan Medical Key Laboratory for Research of Trauma and Orthopedics, the Third Affiliated Hospital of Xinxiang Medical University, Xinxiang453003, China

  • 2.

    Department of Burns and Cutaneous Surgery, Burn Center of PLA, the First Affiliated Hospital of Air Force Medical University, Xi'an710032, China

Funds:

General Program of National Natural Science Foundation of China 82272268

The Open Research Fund of Henan Key Laboratory for Trauma and Orthopedics of Xinxiang Medical University HZKFKT20220503

More Information
  • Corresponding author: Ren Wenjie, Email: xxmu_rwj@163.com
  • Received Date: 2024-05-28
    Abstract
  •   Objective  To investigates the role and mechanism of ferroptosis in combined burn-blast injury with acute lung injury in rats.  Methods  This study was an experimental study. Twenty-four 8-week-old male Sprague-Dawley rats were divided into control group and experimental group by random number table method, each containing 12 animals. The rats in experimental group were anesthetized and subjected to explosion treatment to create the model of combined burn-blast injury with acute lung injury, whereas the rats in control group underwent sham injury. At 24 hours post injury, the pathological morphology of lung tissue was observed by hematoxylin-eosin staining and immunohistochemical staining. The levels of tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), and IL-6 in the supernatant of bronchoalveolar lavage fluid (BALF) were detected by enzyme-linked immunosorbent assay. The arterial partial pressure of oxygen (PaO2) and arterial partial pressure of carbon dioxide (PaCO2) of abdominal aortic blood were measured by automatic animal blood gas analyzer. The lung tissue was weighed and the wet-dry weight ratio was calculated. The total protein concentration in BALF was measured by bicinchoninic acid assay. Lung injury was scored based on hematoxylin-eosin staining. The levels of oxidative stress factors, such as reactive oxygen species, malondialdehyde, superoxide dismutase (SOD), glutathione, and ferrous ion in lung tissue homogenate of rats were detected by related kits. The expression levels of ferroptosis-related molecule glutathione peroxidase 4 (GPX4), lipid peroxidation-related molecule 4-hydroxynonenal (4-HNE), and oxidative DNA damage-related molecule 8-hydroxydeoxyguanosine (8-OHdG) in lung tissue were detected by immunofluorescence and immunohistochemistry methods. Mitochondrial morphology in lung tissue cells was observed under transmission electron microscopy. The sample number was all 6.  Results  At 24 hours post injury, the lung tissue structure of rats in control group was clear and complete, and the alveolar wall was normal; in experimental group, the lung tissue edema of rats was obvious, the alveolar wall became thicker, and the structure was not clear. At 24 hours post injury, compared with those in control group, the levels of TNF-α, IL-1β, and IL-6 in BALF supernatant of rats in experimental group were significantly increased (with t values of 3.96, 9.84, and 10.60, respectively, P<0.05); the wet-dry weight ratio of lung tissue, lung injury score, and total protein concentration in BALF of rats in experimental group were significantly increased (with t values of 6.91, 6.64, and 10.04, respectively, P<0.05), PaO2 of abdominal aortic blood decreased significantly (t=8.85, P<0.05) while PaCO2 did not change significantly (P>0.05); the levels of SOD and glutathione in the lung tissue homogenate of rats in experimental group were significantly decreased (with t values of 4.36 and 8.56, respectively, P<0.05), while the levels of reactive oxygen species, malondialdehyde, and ferrous ion were significantly increased (with t values of 11.55, 9.78, and 14.77, respectively, P<0.05). At 24 hours post injury, immunofluorescence staining and immunohistochemical staining showed that the expression levels of GPX4 in lung tissue of rats in experimental group were 0.245±0.024 and 0.786±0.240, respectively, which were significantly lower than 1.000±0.305 and 1.000±0.200 in control group (with t values of 6.05 and 2.60, respectively, P<0.05); the expression levels of 4-HNE in lung tissue of rats in experimental group were 5.93±1.05 and 2.21±0.23, respectively, which were significantly higher than 1.00±0.29 and 1.00±0.23 in control group (with t values of 11.13 and 9.16, respectively, P<0.05); the expression levels of 8-OHdG in lung tissue of rats in experimental group were 2.08±0.40 and 1.61±0.29, respectively, which were significantly higher than 1.00±0.40 and 1.00±0.26 in control group (with t values of 4.72 and 3.87, respectively, P<0.05). At 24 hours post injury, compared with that in control group, the density of mitochondrial double-layer membrane in the lung tissue cells of rats in experimental group increased, the outer membrane ruptured, and the crista decreased.  Conclusions  In rats with combined burn-blast injury with acute lung injury, there is oxidative DNA damage in lung tissue cells, the imbalance of antioxidant system in lung tissue, and a decrease in the expression of GPX4, the key molecule against ferroptosis, suggesting that ferroptosis is involved in the pathophysiological process of this disease.

     

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