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[Effects of hyperoxia on inflammatory response in lung of infantile rats]
Chang-yi Wu1, Feng Yue, Min Li
1Department of Anesthesiology, Peking University Third Hospital, Beijing 100191, China.
Insights
Exposure to hyperoxia causes lung inflammatory injury in infantile rats. Inflammatory markers like TNF-alpha, IL-6, and IL-10 in BALF peak around 24 hours of oxygen exposure.
Area of Science:
- Pulmonary Medicine
- Neonatology
- Toxicology
Context:
- Infantile rats are susceptible to lung injury from hyperoxia.
- Inflammatory responses play a critical role in hyperoxia-induced lung damage.
Purpose:
- To investigate the impact of hyperoxia on lung inflammation in young rats.
- To quantify inflammatory markers and lung injury scores under varying hyperoxia durations.
Summary:
- Hyperoxia exposure in infantile rats increased malondialdehyde and myeloperoxidase levels, indicating oxidative stress and inflammation.
- Pro-inflammatory cytokines Tumor Necrosis Factor-alpha (TNF-alpha), Interleukin-6 (IL-6), and anti-inflammatory IL-10 in bronchoalveolar lavage fluid (BALF) peaked at 24 hours.
- Lung injury scores progressively worsened with longer hyperoxia exposure.
Impact:
- This study highlights the damaging effects of hyperoxia on developing lungs.
- Findings suggest a critical time window for intervention during hyperoxia therapy in neonates.
Objective:
To investigate the effects of hyperoxia on inflammatory response in lung of infantile rats.
Methods:
Forty 21-day-old male Sprague-Dawley (SD) rats were randomly divided into five groups: room-air control group and 12, 24, 48, 72 hours hyperoxia groups, with the rats continuously exposed to room-air and oxygen (92%-94%) respectively. The rats were sacrificed by depletion method, and lung tissue was obtained for bronchoalveolar lavage. The contents of malondialdehyde (MDA) and the activities of myeloperoxidase (MPO) in lung tissue were assayed by thiobarbituric acid or chromometry, and the concentrations of tumor necrosis factor-alpha (TNF-alpha), interleukin-6 (IL-6) and IL-10 in bronchoalveolar lavage fluid (BALF) were measured by enzyme linked immunosorbent assay (ELISA). The lung pathology was examined, and lung injury score was assessed.
Results:
Compared with the room-air control group, the contents of MDA [(2.24+/-0.43) mmol/g vs. (1.57+/-0.31) mmol/g] and the activities of MPO [(1.24+/-0.25) U/g vs. (0.69+/-0.22) U/g] from lung tissue were elevated at 12 hours and 24 hours of hyperoxia exposure, respectively, and they further increased with prolongation of hyperoxia exposure (P<0.05 or P<0.01). The values of TNF-alpha [(135.2+/-44.0) ng/L vs. (94.5+/-22.3) ng/L], IL-6 [(73.1+/-14.2) ng/L vs. (55.7+/-17.3) ng/L] and IL-10 [(67.9+/-21.7) ng/L vs. (48.2+/-7.6) ng/L] in BALF were all higher at 24 hours of hyperoxia exposure than those of the room-air control group (P<0.05 or P<0.01), but decreased at 48 hours of hyperoxia exposure compared with those of 24-hour hyperoxia exposure group [TNF-alpha: (105.4+/-17.0) ng/L, IL-6: (54.3+/-17.4) ng/L, IL-10: (50.9+/-6.9) ng/L, all P<0.05]. Lung injury scores were higher at 12 hours of hyperoxia exposure as compared with those of the room-air control group (4.5+/-1.4 vs. 1.3+/-0.5), and it further increased with prolongation of hyperoxia exposure (P<0.05 or P<0.01).
Conclusion:
Hyperoxia can lead to lung inflammatory injury in infantile rats, and the expressions of TNF-alpha, IL-6 and IL-10 in BALF may reach the peak at 24 hours of hyperoxia exposure.
