Objective: To investigate the role of high mobility group box 1 (HMGB1) and receptor for advanced glycation end product (RAGE) in the lungs of hyperoxia-induced rats and the effect of N--acetlycystein (NAC).
Methods: A model of hyperoxic lung injury was established, rats in the NAC intervention, and control, hyperoxia group were given nebulized NAC aerosol, nebulized same volume of saline once a day for 7 consecutive days, respectively. Wet/dry ( W/ D) ratio of the lungs was determined to evaluate the edema of the lung tissues. Conventional hematoxylin-eosin (HE) staining was used to observe the pathological changes of lung tissues. Immunohistochemical staining was used to investigate the expression of HMGB1 and RAGE in the lung tissues. Quantitative reverse-transcription polymerase chain reaction and western blot analysis were used to measured the changes in the messenger RNA (mRNA) and protein expression of HMGB1 and RAGE, respectively.
Results: Weight gain of the rats in the hyperoxia group was significantly slower than that in the control group and intervention group (p < 0.05). HE staining results showed lung tissues in the hyperoxia group were severely damaged compared with control group. W/D ratio in hyperoxia group was significantly higher than that in control group and intervention group (p < 0.05). Protein and mRNA expression of HMGB1 and RAGE in the hyperoxia group were significantly higher than control group and intervention group (p < 0.05).
Conclusion: HMGB1 and RAGE were involved in the pathogenesis of hyperoxia-induced lung injury, inhalation of NAC might alleviate hyperoxia-induced lung injury by regulating the expression of HMGB1 and RAGE.
Keywords: N-acetylcysteine; high mobility group box 1; hyperoxia-induced lung injury; receptor for advanced glycation end product.
© 2018 Wiley Periodicals, Inc.