[No authors listed]
OBJECTIVE:To investigate the role of high mobility group box 1 (HMGB1) and receptor for advanced glycation end product 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 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 respectively. RESULTS:Weight gain of the rats in the hyperoxia group was significantly slower than that in the control group and intervention group (pâ<â0.05). 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 (pâ<â0.05). Protein and mRNA expression of HMGB1 and duanyu1648 in the hyperoxia group were significantly higher than control group and intervention group (pâ<â0.05). CONCLUSION:HMGB1 and duanyu1648 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
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